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Border-associated macrophages in the central nervous system J. Neuroinflammation (IF 9.3) Pub Date : 2024-03-13 Rui Sun, Haowu Jiang
Tissue-resident macrophages play an important role in the local maintenance of homeostasis and immune surveillance. In the central nervous system (CNS), brain macrophages are anatomically divided into parenchymal microglia and non-parenchymal border-associated macrophages (BAMs). Among these immune cell populations, microglia have been well-studied for their roles during development as well as in health
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TYROBP/DAP12 knockout in Huntington’s disease Q175 mice cell-autonomously decreases microglial expression of disease-associated genes and non-cell-autonomously mitigates astrogliosis and motor deterioration J. Neuroinflammation (IF 9.3) Pub Date : 2024-03-08 Jordi Creus-Muncunill, Jean Vianney Haure-Mirande, Daniele Mattei, Joanna Bons, Angie V. Ramirez, B. Wade Hamilton, Chuhyon Corwin, Sarah Chowdhury, Birgit Schilling, Lisa M. Ellerby, Michelle E. Ehrlich
Huntington’s disease (HD) is a fatal neurodegenerative disorder caused by an expansion of the CAG trinucleotide repeat in the Huntingtin gene (HTT). Immune activation is abundant in the striatum of HD patients. Detection of active microglia at presymptomatic stages suggests that microgliosis is a key early driver of neuronal dysfunction and degeneration. Recent studies showed that deletion of Tyrobp
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Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions J. Neuroinflammation (IF 9.3) Pub Date : 2024-03-07 Rami A. Shahror, Carol A. Morris, Aya A. Mohammed, Melissa Wild, Bushra Zaman, Christian D. Mitchell, Paul H. Phillips, Nancy J. Rusch, Esraa Shosha, Abdelrahman Y. Fouda
Myeloid cells including microglia and macrophages play crucial roles in retinal homeostasis by clearing cellular debris and regulating inflammation. These cells are activated in several blinding ischemic retinal diseases including diabetic retinopathy, where they may exert both beneficial and detrimental effects on neurovascular function and angiogenesis. Myeloid cells impact the progression of retinal
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The contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome J. Neuroinflammation (IF 9.3) Pub Date : 2024-03-05 Alice Brandli, Kirstan A. Vessey, Erica L. Fletcher
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss, characterised by the dysfunction and death of the photoreceptors and retinal pigment epithelium (RPE). Innate immune cell activation and accompanying para-inflammation have been suggested to contribute to the pathogenesis of AMD, although the exact mechanism(s) and signalling pathways remain elusive. Pattern recognition
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Single-cell RNA sequencing reveals peripheral blood leukocyte responses to spinal cord injury in mice with humanised immune systems J. Neuroinflammation (IF 9.3) Pub Date : 2024-03-01 Ellen R. Gillespie, Laura F. Grice, Isabel G. Courtney, Hong Wa Lao, Woncheol Jung, Sonny Ramkomuth, Jacky Xie, David A. Brown, James Walsham, Kristen J. Radford, Quan H. Nguyen, Marc J. Ruitenberg
Next-generation humanised mouse models and single-cell RNA sequencing (scRNAseq) approaches enable in-depth studies into human immune cell biology. Here we used NSG-SGM3 mice engrafted with human umbilical cord haematopoietic stem cells to investigate how human immune cells respond to and/or are changed by traumatic spinal cord injury (SCI). We hypothesised that the use of such mice could help advance
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Human serum-derived α-synuclein auto-antibodies mediate NMDA receptor-dependent degeneration of CNS neurons J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-28 Pretty Garg, Franziska Würtz, Fabian Hobbie, Klemens Buttgereit, Abhishek Aich, Kristian Leite, Peter Rehling, Sebastian Kügler, Mathias Bähr
Presence of autoantibodies against α-synuclein (α-syn AAb) in serum of the general population has been widely reported. That such peripheral factors may be involved in central nervous system pathophysiology was demonstrated by detection of immunoglobulins (IgGs) in cerebrospinal fluid and brain of Parkinson’s disease (PD) patients. Thus, blood-borne IgGs may reach the brain parenchyma through an impaired
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Inhibition of MMP8 effectively alleviates manic-like behavior and reduces neuroinflammation by modulating astrocytic CEBPD J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-28 Tzu-Yun Wang, Eddie Feng-Ju Weng, Yun-Chen Hsu, Lu-Ping Shiu, Teng-Wei Huang, Hsuan-Cheng Wu, Jau-Shyong Hong, Shao-Ming Wang
There is an intrinsic relationship between psychiatric disorders and neuroinflammation, including bipolar disorder. Ouabain, an inhibitor of Na+/K+-ATPase, has been implicated in the mouse model with manic-like behavior. However, the molecular mechanisms linking neuroinflammation and manic-like behavior require further investigation. CCAAT/Enhancer-Binding Protein Delta (CEBPD) is an inflammatory transcription
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IL-6 from cerebrospinal fluid causes widespread pain via STAT3-mediated astrocytosis in chronic constriction injury of the infraorbital nerve J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-28 Ning Yu, Huan Cui, Sixuan Jin, Penghao Liu, Yehong Fang, Fengrun Sun, Yan Cao, Bo Yuan, Yikuan Xie, Wanru Duan, Chao Ma
The spinal inflammatory signal often spreads to distant segments, accompanied by widespread pain symptom under neuropathological conditions. Multiple cytokines are released into the cerebrospinal fluid (CSF), potentially inducing the activation of an inflammatory cascade at remote segments through CSF flow. However, the detailed alteration of CSF in neuropathic pain and its specific role in widespread
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Elevated SLC7A2 expression is associated with an abnormal neuroinflammatory response and nitrosative stress in Huntington’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-28 Ian D. Gaudet, Hongyuan Xu, Emily Gordon, Gianna A. Cannestro, Michael L. Lu, Jianning Wei
We previously identified solute carrier family 7 member 2 (SLC7A2) as one of the top upregulated genes when normal Huntingtin was deleted. SLC7A2 has a high affinity for l-arginine. Arginine is implicated in inflammatory responses, and SLC7A2 is an important regulator of innate and adaptive immunity in macrophages. Although neuroinflammation is clearly demonstrated in animal models and patients with
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Differential contribution of THIK-1 K+ channels and P2X7 receptors to ATP-mediated neuroinflammation by human microglia J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-26 Ali Rifat, Bernardino Ossola, Roland W. Bürli, Lee A. Dawson, Nicola L. Brice, Anna Rowland, Marina Lizio, Xiao Xu, Keith Page, Pawel Fidzinski, Julia Onken, Martin Holtkamp, Frank L. Heppner, Jörg R. P. Geiger, Christian Madry
Neuroinflammation is highly influenced by microglia, particularly through activation of the NLRP3 inflammasome and subsequent release of IL-1β. Extracellular ATP is a strong activator of NLRP3 by inducing K+ efflux as a key signaling event, suggesting that K+-permeable ion channels could have high therapeutic potential. In microglia, these include ATP-gated THIK-1 K+ channels and P2X7 receptors, but
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SPOCK2 modulates neuropathic pain by interacting with MT1-MMP to regulate astrocytic MMP-2 activation in rats with chronic constriction injury J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-22 Chenglong Wang, Yitong Xu, Miao Xu, Cong Sun, Xiaojiao Zhang, Xueshu Tao, Tao Song
Neuropathic pain (NP) is a kind of intractable pain. The pathogenesis of NP remains a complicated issue for pain management practitioners. SPARC/osteonectin, CWCV, and Kazal-like domains proteoglycan 2 (SPOCK2) are members of the SPOCK family that play a significant role in the development of the central nervous system. In this study, we investigated the role of SPOCK2 in the development of NP in a
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Gliosis-dependent expression of complement factor H truncated variants attenuates retinal neurodegeneration following ischemic injury J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-22 Josef Biber, Yassin Jabri, Sarah Glänzer, Aaron Dort, Patricia Hoffelner, Christoph Q. Schmidt, Oliver Bludau, Diana Pauly, Antje Grosche
Inherited, age-related, and acute retinal diseases are often exacerbated by an aberrant or excessive activity of the complement system. Consequently, cells not directly affected by an acute event or genetic variants may degenerate, resulting in enhanced visual impairment. The therapeutic potential of supplementation of complement factor H (FH), a key regulator of the complement cascade, is therefore
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Dimethyl fumarate improves cognitive impairment and neuroinflammation in mice with Alzheimer’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-21 Ting Wang, Akira Sobue, Seiji Watanabe, Okiru Komine, Takaomi C. Saido, Takashi Saito, Koji Yamanaka
Neuroinflammation substantially contributes to the pathology of Alzheimer’s disease (AD), the most common form of dementia. Studies have reported that nuclear factor erythroid 2-related factor 2 (Nrf2) attenuates neuroinflammation in the mouse models of neurodegenerative diseases, however, the detailed mechanism remains unclear. The effects of dimethyl fumarate (DMF), a clinically used drug to activate
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Parkinson’s disease-derived α-synuclein assemblies combined with chronic-type inflammatory cues promote a neurotoxic microglial phenotype J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-21 Cansu Yildirim-Balatan, Alexis Fenyi, Pierre Besnault, Lina Gomez, Julia E. Sepulveda-Diaz, Patrick P. Michel, Ronald Melki, Stéphane Hunot
Parkinson’s disease (PD) is a common age-related neurodegenerative disorder characterized by the aggregation of α-Synuclein (αSYN) building up intraneuronal inclusions termed Lewy pathology. Mounting evidence suggests that neuron-released αSYN aggregates could be central to microglial activation, which in turn mounts and orchestrates neuroinflammatory processes potentially harmful to neurons. Therefore
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Integration of National Health Insurance claims data and animal models reveals fexofenadine as a promising repurposed drug for Parkinson’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-21 Jae-Bong Kim, Yujeong Kim, Soo-Jeong Kim, Tae‑Young Ha, Dong-Kyu Kim, Dong Won Kim, Minyoung So, Seung Ho Kim, Hyun Goo Woo, Dukyong Yoon, Sang Myun Park
Parkinson’s disease (PD) is a common and costly progressive neurodegenerative disease of unclear etiology. A disease-modifying approach that can directly stop or slow its progression remains a major unmet need in the treatment of PD. A clinical pharmacology-based drug repositioning strategy is a useful approach for identifying new drugs for PD. We analyzed claims data obtained from the National Health
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Combination protein biomarkers predict multiple sclerosis diagnosis and outcomes J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-17 Eleftheria Kodosaki, W. John Watkins, Sam Loveless, Karim L. Kreft, Aidan Richards, Valerie Anderson, Lisa Hurler, Neil P. Robertson, Wioleta M. Zelek, Emma C. Tallantyre
Establishing biomarkers to predict multiple sclerosis diagnosis and prognosis has been challenging using a single biomarker approach. We hypothesised that a combination of biomarkers would increase the accuracy of prediction models to differentiate multiple sclerosis from other neurological disorders and enhance prognostication for people with multiple sclerosis. We measured 24 fluid biomarkers in
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The insular cortex is not insular in thyroid eye disease: neuroimaging revelations of central–peripheral system interaction J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-17 Haiyang Zhang, Yuting Liu, Duojin Xia, Mengda Jiang, Yinwei Li, Jing Sun, Haixia Guan, Ling Zhu, Xuefei Song, Jue Wang, Xianqun Fan, Huifang Zhou
Thyroid eye disease (TED) is highly correlated with dysregulated immunoendocrine status. The insular cortex was found to regulate peripheral inflammation and immunomodulation in mice. This study aimed to explore whether the insular cortex in patients with TED played a modulatory role including the aberrant brain functional alteration and its association with immunoendocrine status. This study included
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Advanced patient-specific microglia cell models for pre-clinical studies in Alzheimer’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-15 Carla Cuní-López, Romal Stewart, Lotta E. Oikari, Tam Hong Nguyen, Tara L. Roberts, Yifan Sun, Christine C. Guo, Michelle K. Lupton, Anthony R. White, Hazel Quek
Alzheimer’s disease (AD) is an incurable neurodegenerative disorder with a rapidly increasing prevalence worldwide. Current approaches targeting hallmark pathological features of AD have had no consistent clinical benefit. Neuroinflammation is a major contributor to neurodegeneration and hence, microglia, the brain’s resident immune cells, are an attractive target for potentially more effective therapeutic
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Intracerebellar injection of monocytic immature myeloid cells prevents the adverse effects caused by stereotactic surgery in a model of cerebellar neurodegeneration J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-14 Carlos del Pilar, Lucía Garrido-Matilla, Lucía del Pozo-Filíu, Rafael Lebrón-Galán, Raúl F. Arias, Diego Clemente, José Ramón Alonso, Eduardo Weruaga, David Díaz
Myeloid-derived suppressor cells (MDSCs) constitute a recently discovered bone-marrow-derived cell type useful for dealing with neuroinflammatory disorders. However, these cells are only formed during inflammatory conditions from immature myeloid cells (IMCs) that acquire immunosuppressive activity, thus being commonly gathered from diseased animals. Then, to obtain a more clinically feasible source
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The role of CD56bright NK cells in neurodegenerative disorders J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-13 Carla Rodriguez-Mogeda, Chaja M. J. van Ansenwoude, Lennart van der Molen, Eva M. M. Strijbis, Reina E. Mebius, Helga E. de Vries
Emerging evidence suggests a potential role for natural killer (NK) cells in neurodegenerative diseases, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. However, the precise function of NK cells in these diseases remains ambiguous. The existence of two NK cell subsets, CD56bright and CD56dim NK cells, complicates the understanding of the contribution
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Progranulin haploinsufficiency mediates cytoplasmic TDP-43 aggregation with lysosomal abnormalities in human microglia J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-13 Wonjae Sung, Min-Young Noh, Minyeop Nahm, Yong Sung Kim, Chang-Seok Ki, Young-Eun Kim, Hee-Jin Kim, Seung Hyun Kim
Progranulin (PGRN) haploinsufficiency due to progranulin gene (GRN) variants can cause frontotemporal dementia (FTD) with aberrant TAR DNA-binding protein 43 (TDP-43) accumulation. Despite microglial burden with TDP-43-related pathophysiology, direct microglial TDP-43 pathology has not been clarified yet, only emphasized in neuronal pathology. Thus, the objective of this study was to investigate TDP-43
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Inflammatory biomarkers for neurobehavioral dysregulation in former American football players: findings from the DIAGNOSE CTE Research Project J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-09 Suzan van Amerongen, Surya V. Pulukuri, Fatima Tuz-Zahra, Yorghos Tripodis, Jonathan D. Cherry, Charles Bernick, Yonas E. Geda, Jennifer V. Wethe, Douglas I. Katz, Michael L. Alosco, Charles H. Adler, Laura J. Balcer, Nicholas J. Ashton, Kaj Blennow, Henrik Zetterberg, Daniel H. Daneshvar, Elizabeth A. Colasurdo, Jeffrey J. Iliff, Gail Li, Elaine R. Peskind, Martha E. Shenton, Eric M. Reiman, Jeffrey
Traumatic encephalopathy syndrome (TES) is defined as the clinical manifestation of the neuropathological entity chronic traumatic encephalopathy (CTE). A core feature of TES is neurobehavioral dysregulation (NBD), a neuropsychiatric syndrome in repetitive head impact (RHI)-exposed individuals, characterized by a poor regulation of emotions/behavior. To discover biological correlates for NBD, we investigated
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Peritoneal sepsis caused by Escherichia coli triggers brainstem inflammation and alters the function of sympatho-respiratory control circuits J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-08 Gjinovefa Kola, Caitlyn W. Clifford, Cara K. Campanaro, Rishi R. Dhingra, Mathias Dutschmann, Frank J. Jacono, Thomas E. Dick
Sepsis has a high mortality rate due to multiple organ failure. However, the influence of peripheral inflammation on brainstem autonomic and respiratory circuits in sepsis is poorly understood. Our working hypothesis is that peripheral inflammation affects central autonomic circuits and consequently contributes to multiorgan failure in sepsis. In an Escherichia coli (E. coli)–fibrin clot model of peritonitis
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Mitochondrial stress: a key role of neuroinflammation in stroke J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-06 Ling Gao, Li Peng, Jian Wang, John H. Zhang, Ying Xia
Stroke is a clinical syndrome characterized by an acute, focal neurological deficit, primarily caused by the occlusion or rupture of cerebral blood vessels. In stroke, neuroinflammation emerges as a pivotal event contributing to neuronal cell death. The occurrence and progression of neuroinflammation entail intricate processes, prominently featuring mitochondrial dysfunction and adaptive responses
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Th1 cells contribute to retinal ganglion cell loss in glaucoma in a VCAM-1-dependent manner J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-05 Chong He, Kun Peng, Xiong Zhu, Zuo Wang, Wenbo Xiu, Gao Zhang, Yang Chen, Chaonan Sun, Xiao Xiao, Donghua Liu, An Li, Yanping Gao, Jinxia Wang, Ping Shuai, Yilian Chen, Ling Yu, Fang Lu
Glaucoma is a complex neurodegenerative disorder characterized by the progressive loss of retinal ganglion cells (RGC) and optic nerve axons, leading to irreversible visual impairment. Despite its clinical significance, the underlying mechanisms of glaucoma pathogenesis remain poorly understood. In this study, we aimed to unravel the multifaceted nature of glaucoma by investigating the interaction
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Fractalkine isoforms differentially regulate microglia-mediated inflammation and enhance visual function in the diabetic retina J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-04 Derek Rodriguez, Kaira A. Church, Alicia N. Pietramale, Sandra M. Cardona, Difernando Vanegas, Colin Rorex, Micah C. Leary, Isabel A. Muzzio, Kevin R. Nash, Astrid E. Cardona
Diabetic retinopathy (DR) affects about 200 million people worldwide, causing leakage of blood components into retinal tissues, leading to activation of microglia, the resident phagocytes of the retina, promoting neuronal and vascular damage. The microglial receptor, CX3CR1, binds to fractalkine (FKN), an anti-inflammatory chemokine that is expressed on neuronal membranes (mFKN), and undergoes constitutive
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Immunoregulatory and neutrophil-like monocyte subsets with distinct single-cell transcriptomic signatures emerge following brain injury J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-03 Erwin K. Gudenschwager Basso, Jing Ju, Eman Soliman, Caroline de Jager, Xiaoran Wei, Kevin J. Pridham, Michelle L. Olsen, Michelle H. Theus
Monocytes represent key cellular elements that contribute to the neurological sequela following brain injury. The current study reveals that trauma induces the augmented release of a transcriptionally distinct CD115+/Ly6Chi monocyte population into the circulation of mice pre-exposed to clodronate depletion conditions. This phenomenon correlates with tissue protection, blood–brain barrier stability
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Exercise mimetics: a novel strategy to combat neuroinflammation and Alzheimer’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-02 Renqing Zhao
Neuroinflammation is a pathological hallmark of Alzheimer’s disease (AD), characterized by the stimulation of resident immune cells of the brain and the penetration of peripheral immune cells. These inflammatory processes facilitate the deposition of amyloid-beta (Aβ) plaques and the abnormal hyperphosphorylation of tau protein. Managing neuroinflammation to restore immune homeostasis and decrease
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Long-term impact of maternal obesity on the gliovascular unit and ephrin signaling in the hippocampus of adult offspring J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-02 Seyedeh Marziyeh Jabbari Shiadeh, Fanny Goretta, Pernilla Svedin, Thomas Jansson, Carina Mallard, Maryam Ardalan
Children born to obese mothers are at increased risk of developing mood disorders and cognitive impairment. Experimental studies have reported structural changes in the brain such as the gliovascular unit as well as activation of neuroinflammatory cells as a part of neuroinflammation processing in aged offspring of obese mothers. However, the molecular mechanisms linking maternal obesity to poor neurodevelopmental
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Herpes simplex virus infection induces necroptosis of neurons and astrocytes in human fetal organotypic brain slice cultures J. Neuroinflammation (IF 9.3) Pub Date : 2024-02-01 Ahmad S. Rashidi, Diana N. Tran, Caithlin R. Peelen, Michiel van Gent, Werner J. D. Ouwendijk, Georges M. G. M. Verjans
Herpes simplex virus (HSV) encephalitis (HSE) is a serious and potentially life-threatening disease, affecting both adults and newborns. Progress in understanding the virus and host factors involved in neonatal HSE has been hampered by the limitations of current brain models that do not fully recapitulate the tissue structure and cell composition of the developing human brain in health and disease
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Preclinical translational platform of neuroinflammatory disease biology relevant to neurodegenerative disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-31 Kelley C. Larson, Lauren H. Martens, Michael Marconi, Christopher Dejesus, Suzanne Bruhn, Thomas A. Miller, Barbara Tate, Jonathan M. Levenson
Neuroinflammation is a key driver of neurodegenerative disease, however the tools available to model this disease biology at the systems level are lacking. We describe a translational drug discovery platform based on organotypic culture of murine cortical brain slices that recapitulate disease-relevant neuroinflammatory biology. After an acute injury response, the brain slices assume a chronic neuroinflammatory
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Enhanced meningeal lymphatic drainage ameliorates lipopolysaccharide-induced brain injury in aged mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-30 Hongquan Dong, Xiaonan Dai, Yin Zhou, Chonglong Shi, Piplu Bhuiyan, Zhaochu Sun, Nana Li, Wenjie Jin
Sepsis-associated encephalopathy (SAE) is an acute cerebral dysfunction caused by sepsis. Neuroinflammation induced by sepsis is considered a potential mechanism of SAE; however, very little is known about the role of the meningeal lymphatic system in SAE. Sepsis was established in male C57BL/6J mice by intraperitoneal injection of 5 mg/kg lipopolysaccharide, and the function of meningeal lymphatic
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SRGN amplifies microglia-mediated neuroinflammation and exacerbates ischemic brain injury J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-29 Yi Qian, Lixuan Yang, Jian Chen, Chao Zhou, Ningning Zong, Yang Geng, Shengnan Xia, Haiyan Yang, Xinyu Bao, Yan Chen, Yun Xu
Microglia is the major contributor of post-stroke neuroinflammation cascade and the crucial cellular target for the treatment of ischemic stroke. Currently, the endogenous mechanism underlying microglial activation following ischemic stroke remains elusive. Serglycin (SRGN) is a proteoglycan expressed in immune cells. Up to now, the role of SRGN on microglial activation and ischemic stroke is largely
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IKKβ deletion from CNS macrophages increases neuronal excitability and accelerates the onset of EAE, while from peripheral macrophages reduces disease severity J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-27 Maria Avloniti, Maria Evangelidou, Maria Gomini, Theodore Loupis, Mary Emmanouil, Adamantia Mitropoulou, Theodore Tselios, Hans Lassmann, Agnès Gruart, José M. Delgado-García, Lesley Probert, Vasiliki Kyrargyri
Multiple sclerosis (MS) is a neuroinflammatory demyelinating disease characterized by motor deficits and cognitive decline. Many immune aspects of the disease are understood through studies in the experimental autoimmune encephalomyelitis (EAE) model, including the contribution of the NF-κB transcription factor to neuroinflammation. However, the cell-specific roles of NF-κB to EAE and its cognitive
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The glucocorticoid receptor as a master regulator of the Müller cell response to diabetic conditions in mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-25 Anna M. Pfaller, Lew Kaplan, Madalena Carido, Felix Grassmann, Nundehui Díaz-Lezama, Farhad Ghaseminejad, Kirsten A. Wunderlich, Sarah Glänzer, Oliver Bludau, Thomas Pannicke, Bernhard H. F. Weber, Susanne F. Koch, Boyan Bonev, Stefanie M. Hauck, Antje Grosche
Diabetic retinopathy (DR) is considered a primarily microvascular complication of diabetes. Müller glia cells are at the centre of the retinal neurovascular unit and play a critical role in DR. We therefore investigated Müller cell-specific signalling pathways that are altered in DR to identify novel targets for gene therapy. Using a multi-omics approach on purified Müller cells from diabetic db/db
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Modeling the neuroimmune system in Alzheimer’s and Parkinson’s diseases J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-23 Wendy Balestri, Ruchi Sharma, Victor A. da Silva, Bianca C. Bobotis, Annabel J. Curle, Vandana Kothakota, Farnoosh Kalantarnia, Maria V. Hangad, Mina Hoorfar, Joanne L. Jones, Marie-Ève Tremblay, Jehan J. El-Jawhari, Stephanie M. Willerth, Yvonne Reinwald
Parkinson’s disease (PD) and Alzheimer’s disease (AD) are neurodegenerative disorders caused by the interaction of genetic, environmental, and familial factors. These diseases have distinct pathologies and symptoms that are linked to specific cell populations in the brain. Notably, the immune system has been implicated in both diseases, with a particular focus on the dysfunction of microglia, the brain’s
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Synergistic effect of sildenafil combined with controlled hypothermia to alleviate microglial activation after neonatal hypoxia–ischemia in rats J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-23 Pansiot Julien, Manuela Zinni, Natacha Bonnel, Marina El Kamouh, Felipe Odorcyk, Lea Peters, Emilie-Fleur Gautier, Marjorie Leduc, Cédric Broussard, Olivier Baud
The only validated treatment to prevent brain damage associated with hypoxia–ischemia (HI) encephalopathy of the newborn is controlled hypothermia with limited benefits. Additional putative neuroprotective drug candidates include sildenafil citrate, a phosphodiesterase-type 5 inhibitor. The main objective of this preclinical study is to assess its ability to reduce HI-induced neuroinflammation, in
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Associations between sex, body mass index and the individual microglial response in Alzheimer’s disease J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-23 Gloria Biechele, Boris-Stephan Rauchmann, Daniel Janowitz, Katharina Buerger, Nicolai Franzmeier, Endy Weidinger, Selim Guersel, Sebastian Schuster, Anika Finze, Stefanie Harris, Simon Lindner, Nathalie L. Albert, Christian Wetzel, Rainer Rupprecht, Axel Rominger, Carla Palleis, Sabrina Katzdobler, Lena Burow, Carolin Kurz, Mirlind Zaganjori, Lena-Katharina Trappmann, Oliver Goldhardt, Timo Grimmer
18-kDa translocator protein position-emission-tomography (TSPO-PET) imaging emerged for in vivo assessment of neuroinflammation in Alzheimer’s disease (AD) research. Sex and obesity effects on TSPO-PET binding have been reported for cognitively normal humans (CN), but such effects have not yet been systematically evaluated in patients with AD. Thus, we aimed to investigate the impact of sex and obesity
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Microglia-derived exosomes modulate myelin regeneration via miR-615-5p/MYRF axis J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-22 Xiao-Yu Ji, Yu-Xin Guo, Li-Bin Wang, Wen-Cheng Wu, Jia-Qi Wang, Jin He, Rui Gao, Javad Rasouli, Meng-Yuan Gao, Zhen-Hai Wang, Dan Xiao, Wei-Feng Zhang, Bogoljub Ciric, Yuan Zhang, Xing Li
Demyelination and failure of remyelination in the central nervous system (CNS) characterize a number of neurological disorders. Spontaneous remyelination in demyelinating diseases is limited, as oligodendrocyte precursor cells (OPCs), which are often present in demyelinated lesions in abundance, mostly fail to differentiate into oligodendrocytes, the myelinating cells in the CNS. In addition to OPCs
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Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-20 Peng-Fei Wang, Fei Jiang, Qiu-Ming Zeng, Wei-Fan Yin, Yue-Zi Hu, Qiao Li, Zhao-Lan Hu
Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by the infiltration of inflammatory cells and demyelination of nerves. Mitochondrial dysfunction has been implicated in the pathogenesis of MS, as studies have shown abnormalities in mitochondrial activities, metabolism, mitochondrial DNA (mtDNA) levels, and mitochondrial morphology in immune cells of individuals with MS. The presence
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Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-19 Shutian Zhang, Dajun Zhao, Zhaohua Yang, Fanshun Wang, Shouguo Yang, Chunsheng Wang
Sympathoexcitation contributes to myocardial remodeling in heart failure (HF). Increased circulating pro-inflammatory mediators directly act on the Subfornical organ (SFO), the cardiovascular autonomic center, to increase sympathetic outflow. Circulating mitochondria (C-Mito) are the novel discovered mediators for inter-organ communication. Cyclic GMP–AMP synthase (cGAS) is the pro-inflammatory sensor
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Increased regulatory activity of intestinal innate lymphoid cells type 3 (ILC3) prevents experimental autoimmune encephalomyelitis severity J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-18 Milica Lazarević, Goran Stegnjaić, Bojan Jevtić, Sanja Despotović, Đurđica Ignjatović, Suzana Stanisavljević, Neda Nikolovski, Miljana Momčilović, Graeme L. Fraser, Mirjana Dimitrijević, Đorđe Miljković
Experimental autoimmune encephalomyelitis (EAE) induced in inbred rodents, i.e., genetically identical animals kept under identical environmental conditions, shows variable clinical outcomes. We investigated such variations of EAE in Dark Agouti rats immunized with spinal cord homogenate and identified four groups: lethal, severe, moderate, and mild, at day 28 post immunization. Higher numbers of CD4+
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Repeated cold stress, an animal model for fibromyalgia, elicits proprioceptor-induced chronic pain with microglial activation in mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-18 Koji Wakatsuki, Sumiko Kiryu-Seo, Masaya Yasui, Hiroki Yokota, Haruku Kida, Hiroyuki Konishi, Hiroshi Kiyama
Fibromyalgia is characterized by chronic pain, fatigue, and other somatic symptoms. We have recently revealed that proprioceptor hyperactivation induces chronic pain in a rat model of myalgic encephalomyelitis. The present study explores whether similar proprioceptor-induced pain is elicited in a mouse model of fibromyalgia. Repeated cold stress (RCS) was used as a fibromyalgia model. Pain behavior
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Post-exposure intranasal IFNα suppresses replication and neuroinvasion of Venezuelan Equine Encephalitis virus within olfactory sensory neurons J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-17 Matthew D. Cain, N. Rubin Klein, Xiaoping Jiang, Hamid Salimi, Qingping Wu, Mark J. Miller, William B. Klimstra, Robyn S. Klein
Venezuelan Equine Encephalitis virus (VEEV) may enter the central nervous system (CNS) within olfactory sensory neurons (OSN) that originate in the nasal cavity after intranasal exposure. While it is known that VEEV has evolved several mechanisms to inhibit type I interferon (IFN) signaling within infected cells, whether this inhibits virologic control during neuroinvasion along OSN has not been studied
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Transient immune activation without loss of intraepidermal innervation and associated Schwann cells in patients with complex regional pain syndrome J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-17 Beate Hartmannsberger, Sabrina Scriba, Carolina Guidolin, Juliane Becker, Katharina Mehling, Kathrin Doppler, Claudia Sommer, Heike L. Rittner
Complex regional pain syndrome (CRPS) develops after injury and is characterized by disproportionate pain, oedema, and functional loss. CRPS has clinical signs of neuropathy as well as neurogenic inflammation. Here, we asked whether skin biopsies could be used to differentiate the contribution of these two systems to ultimately guide therapy. To this end, the cutaneous sensory system including nerve
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Splenic monocytes drive pathogenic subretinal inflammation in age-related macular degeneration J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-17 Christophe Roubeix, Caroline Nous, Sébastien Augustin, Kaitryn E. Ronning, Thibaud Mathis, Frédéric Blond, Pauline Lagouge-Roussey, Sergio Crespo-Garcia, Patrick M. Sullivan, Emmanuel L. Gautier, Nadine Reichhart, José-Alain Sahel, Marie E. Burns, Michel Paques, Torben Lykke Sørensen, Olaf Strauss, Xavier Guillonneau, Cécile Delarasse, Florian Sennlaub
Age-related macular degeneration (AMD) is invariably associated with the chronic accumulation of activated mononuclear phagocytes in the subretinal space. The mononuclear phagocytes are composed of microglial cells but also of monocyte-derived cells, which promote photoreceptor degeneration and choroidal neovascularization. Infiltrating blood monocytes can originate directly from bone marrow, but also
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Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression? J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-17 Jelle Y. Broos, Rianne T. M. van der Burgt, Julia Konings, Merel Rijnsburger, Oliver Werz, Helga E. de Vries, Martin Giera, Gijs Kooij
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS), characterized by neuroinflammation, demyelination, and neurodegeneration. Considering the increasing prevalence among young adults worldwide and the disabling phenotype of the disease, a deeper understanding of the complexity of the disease pathogenesis is needed to ultimately improve diagnosis and personalize
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Correction: Glyphosate infiltrates the brain and increases pro-inflammatory cytokine TNFα: implications for neurodegenerative disorders J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-17 Joanna K. Winstone, Khyatiben V. Pathak, Wendy Winslow, Ignazio S. Piras, Jennifer White, Ritin Sharma, Matthew J. Huentelman, Patrick Pirrotte, Ramon Velazquez
Correction: Journal of Neuroinflammation (2022) 19:193 https://doi.org/10.1186/s12974-022-02544-5 Following publication of the original article [1], the authors identified an error in the notation of units used in the publication. All glyphosate and AMPA measurements reported for brain tissue should have been reported as ng/g, instead of ng/mg. This change impacts the axis labels on Fig. 1B, C, E,
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Taming microglia: the promise of engineered microglia in treating neurological diseases J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-11 Echo Yongqi Luo, Rio Ryohichi Sugimura
Microglia, the CNS-resident immune cells, are implicated in many neurological diseases. Nearly one in six of the world’s population suffers from neurological disorders, encompassing neurodegenerative and neuroautoimmune diseases, most with dysregulated neuroinflammation involved. Activated microglia become phagocytotic and secret various immune molecules, which are mediators of the brain immune microenvironment
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Lipoxins A4 and B4 inhibit glial cell activation via CXCR3 signaling in acute retinal neuroinflammation J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-11 Izhar Livne-Bar, Shubham Maurya, Karsten Gronert, Jeremy M. Sivak
Lipoxins are small lipids that are potent endogenous mediators of systemic inflammation resolution in a variety of diseases. We previously reported that Lipoxins A4 and B4 (LXA4 and LXB4) have protective activities against neurodegenerative injury. Yet, lipoxin activities and downstream signaling in neuroinflammatory processes are not well understood. Here, we utilized a model of posterior uveitis
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CD4 T-cell aging exacerbates neuroinflammation in a late-onset mouse model of amyotrophic lateral sclerosis J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-11 Shir Zaccai, Anna Nemirovsky, Livnat Lerner, Leenor Alfahel, Ekaterina Eremenko, Adrian Israelson, Alon Monsonego
Amyotrophic lateral sclerosis (ALS) is an adult-onset progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons in the brain and spinal cord. Accumulating evidence suggests that ALS is not solely a neuronal cell- or brain tissue-autonomous disease and that neuroinflammation plays a key role in disease progression. Furthermore, whereas both CD4 and CD8 T cells
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Chorioamnionitis accelerates granule cell and oligodendrocyte maturation in the cerebellum of preterm nonhuman primates J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-10 Josef Newman, Xiaoying Tong, April Tan, Toni Yeasky, Vanessa Nunes De Paiva, Pietro Presicce, Paranthaman S. Kannan, Kevin Williams, Andreas Damianos, Marione Tamase Newsam, Merline K. Benny, Shu Wu, Karen C. Young, Lisa A. Miller, Suhas G. Kallapur, Claire A. Chougnet, Alan H. Jobe, Roberta Brambilla, Augusto F. Schmidt
Preterm birth is often associated with chorioamnionitis and leads to increased risk of neurodevelopmental disorders, such as autism. Preterm birth can lead to cerebellar underdevelopment, but the mechanisms of disrupted cerebellar development in preterm infants are not well understood. The cerebellum is consistently affected in people with autism spectrum disorders, showing reduction of Purkinje cells
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Hepcidin deficiency impairs hippocampal neurogenesis and mediates brain atrophy and memory decline in mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-09 Xue Bai, Bing Wang, Yiduo Cui, Siqi Tian, Yi Zhang, Linhao You, Yan-Zhong Chang, Guofen Gao
Hepcidin is the master regulator of iron homeostasis. Hepcidin downregulation has been demonstrated in the brains of Alzheimer’s disease (AD) patients. However, the mechanism underlying the role of hepcidin downregulation in cognitive impairment has not been elucidated. In the present study, we generated GFAP-Cre-mediated hepcidin conditional knockout mice (HampGFAP cKO) to explore the effect of hepcidin
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A pre-existing Toxoplasma gondii infection exacerbates the pathophysiological response and extent of brain damage after traumatic brain injury in mice J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-09 Tamara L. Baker, David K. Wright, Alessandro D. Uboldi, Christopher J. Tonkin, Anh Vo, Trevor Wilson, Stuart J. McDonald, Richelle Mychasiuk, Bridgette D. Semple, Mujun Sun, Sandy R. Shultz
Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result
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The microRNA-211-5p/P2RX7/ERK/GPX4 axis regulates epilepsy-associated neuronal ferroptosis and oxidative stress J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-08 Xueying Li, Pusheng Quan, Yao Si, Fei Liu, Yuwei Fan, Feifan Ding, Lina Sun, Han Liu, Shuo Huang, Linlin Sun, Fan Yang, Lifen Yao
Ferroptosis is an iron-dependent cell death mechanism involving the accumulation of lipid peroxides. As a critical regulator, glutathione peroxidase 4 (GPX4) has been demonstrated to be downregulated in epilepsy. However, the mechanism of ferroptosis in epilepsy remains unclear. In this study, bioinformatics analysis, analysis of epilepsy patient blood samples and cell and mouse experiments revealed
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Autoimmune demyelination alters hypothalamic transcriptome and endocrine function J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-04 Jonathan J. Carver, Kristy M. Lau, Alexandra E. Puckett, Alessandro Didonna
The hypothalamus is a brain structure that is deputed to maintain organism homeostasis by regulating autonomic function and hormonal production as part of the neuroendocrine system. Dysfunction in hypothalamic activity results in behavioral alterations, depression, metabolic syndromes, fatigue, and infertility. Remarkably, many of these symptoms are associated with multiple sclerosis (MS), a chronic
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Doxycycline for transgene control disrupts gut microbiome diversity without compromising acute neuroinflammatory response J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-04 Emily J. Koller, Caleb A. Wood, Zoe Lai, Ella Borgenheimer, Kristi L. Hoffman, Joanna L. Jankowsky
The tetracycline transactivator (tTA) system provides controllable transgene expression through oral administration of the broad-spectrum antibiotic doxycycline. Antibiotic treatment for transgene control in mouse models of disease might have undesirable systemic effects resulting from changes in the gut microbiome. Here we assessed the impact of doxycycline on gut microbiome diversity in a tTA-controlled
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Impaired cerebral microvascular endothelial cells integrity due to elevated dopamine in myasthenic model J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-04 Yue Hao, Yinchun Su, Yifan He, Wenyuan Zhang, Yang Liu, Yu Guo, Xingfan Chen, Chunhan Liu, Siyu Han, Buyi Wang, Yushuang Liu, Wei Zhao, Lili Mu, Jinghua Wang, Haisheng Peng, Junwei Han, Qingfei Kong
Myasthenia gravis is an autoimmune disease characterized by pathogenic antibodies that target structures of the neuromuscular junction. However, some patients also experience autonomic dysfunction, anxiety, depression, and other neurological symptoms, suggesting the complex nature of the neurological manifestations. With the aim of explaining the symptoms related to the central nervous system, we utilized
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Commonly disrupted pathways in brain and kidney in a pig model of systemic endotoxemia J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-04 Kimberly C. Olney, Camila de Ávila, Kennedi T. Todd, Lauren E. Tallant, J. Hudson Barnett, Katelin A. Gibson, Piyush Hota, Adithya Shyamala Pandiane, Pinar Cay Durgun, Michael Serhan, Ran Wang, Mary Laura Lind, Erica Forzani, Naomi M. Gades, Leslie F. Thomas, John D. Fryer
Sepsis is a life-threatening state that arises due to a hyperactive inflammatory response stimulated by infection and rarely other insults (e.g., non-infections tissue injury). Although changes in several proinflammatory cytokines and signals are documented in humans and small animal models, far less is known about responses within affected tissues of large animal models. We sought to understand the
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MIF contribution to progressive brain diseases J. Neuroinflammation (IF 9.3) Pub Date : 2024-01-04 Agata Matejuk, Gil Benedek, Richard Bucala, Szymon Matejuk, Halina Offner, Arthur A. Vandenbark
Progressive brain diseases create a huge social and economic burden on modern societies as a major cause of disability and death. Incidence of brain diseases has a significantly increasing trend and merits new therapeutic strategies. At the base of many progressive brain malfunctions is a process of unresolved, chronic inflammation. Macrophage migration inhibitory factor, MIF, is an inflammatory mediator