Editorial overview: Purinergic P2X receptors in innate immunity and inflammation

doi:10.1016/j.coph.2019.05.003

Current Opinion in Pharmacology

Volume 47, August 2019, Pages 141-144

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Purinergic signaling and gene expression of purinoceptors in the head kidney of the silver catfish Rhamdia quelen experimentally infected by Flavobacterium columnare
2020, Microbial Pathogenesis
Citation Excerpt :
Nevertheless, the mechanisms involved in augmentation of pro-inflammatory cytokines remain unknown, including the involvement of purinergic signaling that can display anti- or pro-inflammatory profiles depending on the type of pathogen, virulence, and severity of infection [13,14]. Purinergic signaling, via the interaction of purine nucleotides (adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP)) or nucleoside (adenosine (Ado)) with the purine receptors present in the plasma membrane of immune tissues, has been associated with prevention of exacerbated immunosuppression and unregulated inflammation [15,16]. There is a multi-enzymatic complex anchored in the plasma membrane of head kidney cells that includes triphosphate diphosphohydrolase (NTPDase), 5′-nucleotidase and adenosine deaminase (ADA) [17].
The head kidney is a lymphoid immune organ that plays a key role in the immune and inflammatory responses of teleost fish. It is associated with immunoglobulin G production and differentiation of B cells. The presence of a multi-enzymatic complex found anchored in the plasma membrane makes the head kidney an important purinergic-dependent tissue. Purinergic signaling has been associated with these responses under pathological conditions via regulation of extracellular adenosine triphosphate (ATP), the main damage molecular associated pattern agent released during bacterial infections. The aim of this study was to determine whether purinergic signaling is a pathway associated with impairment of immune responses in silver catfish (Rhamdia quelen) experimentally infected by Flavobacterium columnare, as well as to evaluate the role of P2 purine receptors in this response. Triphosphate diphosphohydrolase (NTPDase) activity in the head kidney was significantly lower in silver catfish experimentally-infected F. columnare 72 h post-infection (hpi) than in the control group, while no significant difference was observed with respect NTPDase activity on adenosine diphosphate, as well as on 5′-nucleotidase and adenosine deaminase activities. Extracellular ATP levels were significantly higher in the head kidney of experimentally-infected fish than in the control group at 72 hpi. Finally, p2ry11 and p2rx3 purine receptor levels were significantly higher in experimentally-infected fish than in the control group at 72 hpi. We conclude that purinergic signaling in the head kidney of silver catfish infected by F. columnare creates a pro-inflammatory profile that may contribute to impairment of immune and inflammatory responses via reduction of ATP hydrolysis and its accumulation in the extracellular milieu, accompanied by upregulation of p2ry11 and p2rx3 purine receptors, leading to pro-inflammatory status.
Role of CD39 in COVID-19 Severity: Dysregulation of Purinergic Signaling and Thromboinflammation
2022, Frontiers in Immunology
Targeting Purinergic Signaling in the Dynamics of Disease Progression in Sepsis
2021, Frontiers in Pharmacology
The P2X7 purinergic receptor: a potential therapeutic target for lung cancer
2020, Journal of Cancer Research and Clinical Oncology

Dr Di Virgilio is currently Professor of Clinical Pathology, Director of the Post-Graduate Course in Clinical Pathology and Chairman of the PhD Course in Molecular Medicine at the University of Ferrara. He graduated in Medicine at the University of Padova in 1979, and then moved as a Honorary Research Assistant to the University College London (UCL), and later as a Visiting Scientist to Columbia University (New York), where he specialized in the physiology of extracellular ATP and in the biology of macrophages. He set up his own laboratory first at the University of Padova in 1987, and then at the University of Ferrara in 1992. Dr Di Virgilio’s research mainly focused on the identification of the pathophysiological role of the P2X7 receptor, and on the development of probes suitable for the in vivo measurement of extracellular ATP. Dr Di Virgilio is a member of the Committee for Receptor Nomenclature, International Union of Pharmacology (IUPHAR, P2X receptor subcommittee), of the Faculty of 1000 (Cell Biology Section), the European Academy of Tumor Immunology, and the Academia Europea. He has been a consultant with Janssen Pharmaceuticals (Belgium), and a member of the Scientific Advisory Boards (SABs) of Duska Therapeutics Inc (USA) and Affectis Pharmaceuticals AG (Germany). Currently, Dr Di Virgilio is a member the SAB of Biosceptre Ltd (UK).

Dr Pelegrín is deputy Director of the Biomedical Research Institute of Murcia IMIB-Arrixaca, as well as Principal Investigator. He obtained his PhD in the field of comparative immunology at the University of Murcia in Spain with a thesis on the cloning of interleukin-1 from different fish species. He then moved to the University of Sheffield (UK) for a postdoc funded by AstraZeneca, after which he completed a second postdoc at the University of Manchester (UK). During this time, he specialized in the physiology of P2X7 receptors in myeloid cells. He then returned to Murcia where he set up a laboratory to investigate the molecular regulation of inflammation and, in particular, to focus on how the activation of the NLRP3 inflammasome by danger signals is a pathophysiological process in different inflammatory diseases. His research specializes in purinergic signaling through the P2X7 ion-channel receptor in innate immune cells, and how ionic flow across P2X7 modulates the assembly of NLRP3 inflammasome and the unconventional release of pro-inflammatory cytokines of the interleukin-1 family.

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