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Probiotic Lactobacillus and Bifidobacterium Strains Counteract Adherent-Invasive Escherichia coli (AIEC) Virulence and Hamper IL-23/Th17 Axis in Ulcerative Colitis, but Not in Crohn's Disease.
Cells ( IF 6 ) Pub Date : 2020-08-01 , DOI: 10.3390/cells9081824
Gabriella Leccese 1 , Alessia Bibi 1 , Stefano Mazza 2 , Federica Facciotti 3 , Flavio Caprioli 2, 4 , Paolo Landini 1 , Moira Paroni 1
Affiliation  

Hypersecretion of proinflammatory cytokines and dysregulated activation of the IL-23/Th17 axis in response to intestinal microbiota dysbiosis are key factors in the pathogenesis of inflammatory bowel diseases (IBD). In this work, we studied how Lactobacillus and Bifidobacterium strains affect AIEC-LF82 virulence mechanisms and the consequent inflammatory response linked to the CCR6–CCL20 and IL-23/Th17 axes in Crohn’s disease (CD) and ulcerative colitis (UC) patients. All Lactobacillus and Bifidobacterium strains significantly reduced the LF82 adhesion and persistence within HT29 intestinal epithelial cells, inhibiting IL-8 secretion while not affecting the CCR6–CCL20 axis. Moreover, they significantly reduced LF82 survival within macrophages and dendritic cells, reducing the secretion of polarizing cytokines related to the IL-23/Th17 axis, both in healthy donors (HD) and UC patients. In CD patients, however, only B. breve Bbr8 strain was able to slightly reduce the LF82 persistence within dendritic cells, thus hampering the IL-23/Th17 axis. In addition, probiotic strains were able to modulate the AIEC-induced inflammation in HD, reducing TNF-α and increasing IL-10 secretion by macrophages, but failed to do so in IBD patients. Interestingly, the probiotic strains studied in this work were all able to interfere with the IL-23/Th17 axis in UC patients, but not in CD patients. The different interaction mechanisms of probiotic strains with innate immune cells from UC and CD patients compared to HD suggest that testing on CD-derived immune cells may be pivotal for the identification of novel probiotic strains that could be effective also for CD patients.

中文翻译:

益生菌乳酸菌和双歧杆菌菌株可抵消溃疡性结肠炎中黏附性侵袭性大肠杆菌(AIEC)的毒力并妨碍IL-23 / Th17轴,但在克罗恩病中则不然。

促炎性细胞因子的过度分泌和肠微生物群失调对IL-23 / Th17轴的活化失调是炎症性肠病(IBD)发病机理的关键因素。在这项工作中,我们研究了乳酸杆菌双歧杆菌菌株如何影响AIEC-LF82毒力机制以及随之而来的炎症反应,这些炎症反应与克罗恩病(CD)和溃疡性结肠炎(UC)患者中的CCR6-CCL20和IL-23 / Th17轴相关。所有乳杆菌双歧杆菌菌株显着降低了HT82肠上皮细胞内的LF82粘附和持久性,抑制了IL-8分泌,同时不影响CCR6-CCL20轴。此外,它们显着降低了巨噬细胞和树突状细胞中LF82的存活率,从而减少了健康供体(HD)和UC患者中与IL-23 / Th17轴相关的极化细胞因子的分泌。然而,在CD患者中,只有短小芽孢杆菌Bbr8菌株能够稍微降低树突状细胞内的LF82持久性,从而阻碍了IL-23 / Th17轴。此外,益生菌菌株能够调节AIEC诱导的HD炎症,减少巨噬细胞的TNF-α并增加IL-10分泌,但在IBD患者中却不能。有趣的是,这项工作中研究的益生菌菌株均能够干扰UC患者的IL-23 / Th17轴,但不会干扰CD患者。与HD相比,益生菌菌株与来自UC和CD患者的先天免疫细胞的不同相互作用机制表明,对CD衍生的免疫细胞进行测试对于鉴定对CD患者也有效的新型益生菌菌株可能至关重要。
更新日期:2020-08-01
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