B cells fulfill multifaceted functions that influence immune responses during health and disease. In autoimmune diseases, such as inflammatory bowel disease, multiple sclerosis and rheumatoid arthritis, depletion of functional B cells results in an aggravation of disease in humans and respective mouse models. This could be due to a lack of a pivotal B cell subpopulation: regulatory B cells (Bregs). Although Bregs represent only a small proportion of all immune cells, they exhibit critical properties in regulating immune responses, thus contributing to the maintenance of immune homeostasis in healthy individuals. In this study, we report that the induction of Bregs is differentially triggered by the immunogenicity of the host microbiota. In comparative experiments with low immunogenic Bacteroides vulgatus and strong immunogenic Escherichia coli, we found that the induction and longevity of Bregs depend on strong Toll-like receptor activation mediated by antigens of strong immunogenic commensals. The potent B cell stimulation via E. coli led to a pronounced expression of suppressive molecules on the B cell surface and an increased production of anti-inflammatory cytokines like interleukin-10. These bacteria-primed Bregs were capable of efficiently inhibiting the maturation and function of dendritic cells (DCs), preventing the proliferation and polarization of T helper (Th)1 and Th17 cells while simultaneously promoting Th2 cell differentiation in vitro. In addition, Bregs facilitated the development of regulatory T cells (Tregs) resulting in a possible feedback cooperation to establish immune homeostasis. Moreover, the colonization of germfree wild type mice with E. coli but not B. vulgatus significantly reduced intestinal inflammatory processes in dextran sulfate sodium (DSS)-induced colitis associated with an increase induction of immune suppressive Bregs. The quantity of Bregs directly correlated with the severity of inflammation. These findings may provide new insights and therapeutic approaches for B cell-controlled treatments of microbiota-driven autoimmune disease.

/pdf/bacterial-immunogenicity-is-critical-for-the-induction-of-vz1njs3ysa.pdf

Bacterial Immunogenicity Is Critical for the Induction of Regulatory B Cells in Suppressing Inflammatory Immune Responses.

Potential role of ovomucin and its peptides in modulation of intestinal health: A review.

Gut microbiota imbalances play an important role in inflammatory bowel disease (IBD), but no single pathogenic microorganism critical to IBD that is specific to the IBD terminal ileum mucosa or can invade intestinal epithelial cells has been found. Invasive Escherichia coli (E. coli) adhesion to macrophages is considered to be closely related to the pathogenesis of inflammatory bowel disease. Further study of the specific biological characteristics of adherent invasive E. coli (AIEC) may contribute to a further understanding of IBD pathogenesis. This review explores the relationship between AIEC and the intestinal immune system, discusses the prevalence and relevance of AIEC in Crohn's disease and ulcerative colitis patients, and describes the relationship between AIEC and the disease site, activity, and postoperative recurrence. Finally, we highlight potential therapeutic strategies to attenuate AIEC colonization in the intestinal mucosa, including the use of phage therapy, antibiotics, and anti-adhesion molecules. These strategies may open up new avenues for the prevention and treatment of IBD in the future.

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

https://link.springer.com/content/pdf/10.1007/s13659-023-00375-2.pdf

Protective effect and mechanism insight of purified Antarctic krill phospholipids against mice ulcerative colitis combined with bioinformatics

Gut microbiota have a role in several diseases, but the exact mechanism of their action is not clear. Gut microbiota synthesizes the short-chain fatty acids (SCFAs) acetate, butyrate, and palmitate, enhances gut serotonin synthesis in collaboration with colonic enterochromaffin cells, and modulates vagal tone. Dietary essential fatty acids (EFAs) and their metabolites are critical for many physiological cellular processes. There are many overlapping actions between gut microbiota and EFAs and their metabolites implying that some close interaction exists among them. EFAs and their metabolites enhance the proliferation of useful gut microbiota, augment gut microbiota production of SCFAs and microbiota, and convert EFAs to SCFAs. This interaction between EFAs and gut microbiota may account for the plethora of actions of EFAs and the gut microbiome in health and disease.

Bioactive lipids and gut microbiota interact to regulate health and disease

Increasing evidence suggests that intestinal microbiota have critical function in the pathogenesis of inflammatory bowel disease. This present study investigated the effects of Escherichia coli (E. coli) in mice with dextran sulfate sodium (DSS)-induced colitis. Furthermore, Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) gene expression was measured by reverse transcription-quantitative polymerase chain reaction. In total, two experiments were performed. In the first experiment, four groups were established in BALB/c mice: i) Group A, control (no treatments); ii) group B, DSS-induced colitis; iii) group C, DSS-induced colitis bacteria depleted (BD) mice; and iv) group D, E. coli-treated DSS-induced colitis BD mice. In the second experiment, there were three groups: i) Group A1, control C57BL/6 mice; ii) group B1, E. coli-treated DSS-induced colitis BD C57BL/6 mice; and iii) E. coli-treated DSS-induced colitis BD TLR4−/− mice. Clinical outcomes, colon and immune histopathology and tissue myeloperoxidase activity were assessed. Mice with DSS-induced colitis that were treated with E. coli exhibited enhanced recovery, with significantly improved clinical and histological scores compared with the DSS only group. The mRNA expression of TLR4 and NF-κB in the E. coli-treated group was also significantly higher. These effects were abolished in TLR4−/− mice, suggesting that E. coli may have promoted recovery through the TLR4 pathway. The present study indicated that E. coli promoted recovery from DSS-induced colitis in mice, potentially through activation of the TLR4/NF-κB signaling pathway.

https://www.spandidos-publications.com/10.3892/mmr.2019.9848/download

Escherichia coli promotes DSS‑induced murine colitis recovery through activation of the TLR4/NF‑κB signaling pathway

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Escherichia coli promotes DSS‑induced murine colitis recovery through activation of the TLR4/NF‑κB signaling pathway