ABSTRACT: Encounter with commensal microbiota is essential for development immune system: comparison of gnotobiote mice with diferent colonization ptorocols (CBX256)
Project description:Commensal bacteria are crucial in maintaining host physiological homeostasis, immune system development, and protection against pathogens. Despite their significance, the factors influencing persistent bacterial colonization and their impact on the host still need to be fully understood. Animal models have served as valuable tools to investigate these interactions, but most have limitations. The bacterial genus Neisseria, which includes both commensal and pathogenic species, has been studied from a pathogenicity to humans’ perspective, but lacks models that study immune responses in the context of long-term persistence. Neisseria musculi, a recently described natural commensal of mice, offers a unique opportunity to study long-term host-commensal interactions. In this study, for the first time we have used this model to study the transcriptional, phenotypic, and functional dynamics of immune cell signatures in the mucosal and systemic tissue of mice in response to Neisseria musculi colonization. We found key genes and pathways vital for immune homeostasis in palate tissue, validated by flow cytometry of immune cells from lung, blood and spleen. This study offers a novel avenue for advancing our understanding of host-bacteria dynamics and may provide a platform for developing efficacious interventions against mucosal persistence by pathogenic Neisseria.
Project description:Commensal bacteria shape the gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms are not yet known. To reveal the mechanism, we isolated naïve CD4+ T cells from the spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Naïve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.
Project description:Commensal bacteria shape the gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms are not yet known. To reveal the mechanism, we isolated naïve CD4+ T cells from the spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria. Naïve T cells were isolated from spleen and were cultured in the presence of IL-2, TGF-beta and in the presence or absene of Butyrate. RNA was extracted at Day 2.
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis.
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis.
Project description:Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition.
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis. Colonic lamina propria cells were isolated from mice described above. Cells were divided into Treg or Non-Treg cells by FACS AriaIII
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated NaM-CM-/ve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria. NaM-CM-/ve T cells were isolated from spleen and were cultured in the presence of IL-2, TGF-beta and in the presence or absene of Butyrate. RNA was extracted at Day 2
Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Treg cells and Non-Treg cells and performed the global expression analysis. Colonic lamina propria cells were isolated from mice described above. Treg cells and Non-Treg cells (also called as Tconv cells) were sorted by FACS AriaIII
