Polymorphic immune mechanisms regulate commensal repertoire
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ABSTRACT:
PROVIDER: PRJNA562711 | ENA |
REPOSITORIES: ENA
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Project description:Environmental influences such as infections and dietary changes strongly affect a host’s microbiota. In the steady state, however, host genetics may influence the microbiota composition, as suggested by the greater similarity between the microbiomes of identical twin pairs compared to non-identical twins. Understanding the role of polymorphic mechanisms in regulating the commensal communities is complicated by the variability of human genomes and microbiomes, and by microbial sensitivity to the environment. Animal studies allow genetic modifications, but are also sensitive to influences known as ‘cage’ or ‘legacy’ effects. Here, we analyzed ex-germ-free mice of various genetic backgrounds, including immunodeficient and Major Histocompatibility Complex (MHC)-congenic strains repopulated with identical input microbiota. We found that the host’s genetic polymorphic mechanisms did indeed affect the gut microbiome and that both innate (e.g. anti-microbial peptides, complement, pentraxins and enzymes affecting microbial survival), as well as adaptive (both MHC-dependent and MHC-independent) pathways influenced the microbiota. These polymorphic mechanisms regulated only a limited number of microbial lineages (independently of their abundance). In addition, our comparative analyses suggested that some microbes might benefit from the specific immune responses that they elicit.
2019-08-29 | GSE136572 | GEO
Project description: Not available
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Project description:Colonizing commensal bacteria after birth are required for the proper development of the gastrointestinal tract. It is believed that bacterial colonization pattern in neonatal gut affects gut barrier function and immune system maturation. Studies on the development of faecal flora microbiota in infants on various formula feeds showed that the neonatal gut was first colonized with enterococci followed by other flora microbiota such as Bifidobacterium in breast feeding infants. Intriguingly, Bjorksten group Other studies showed that Bbabies who developed allergy were less often colonized with Enterococcus during the first month of life as compared to healthy infants. A lot of Many studies have been done on conducted to elucidate how bifidobacteria or lactobacilli, some of which are considered probiotic, regulate infant gut immunity. However, much fewer studies have been focused on enterococi. In our study, we demonstrate that E. faecalis, isolated from healthy newborns, suppress inflammatory responses activated in vivo and in vitro. We found E. faecalis attenuates proinflammatory cytokine secretions, especially IL-8, through JNK and p38 signaling pathways. This finding shed light on how the first colonizer, E.faecalis, regulate inflammatory responses in the host. Samples are analysed using web-based GEArray Expression Analysis Suite
2014-04-04 | E-GEOD-56485 | biostudies-arrayexpress
Project description:Polymorphic integrations of endogenous retroviruses (ERVs) have been previously detected in mouse and human genomes. While most are inert, a subset is capable of influencing the activity of the host genes. However, the molecular mechanism underlying how such elements affect the epigenome and transcriptome and their roles in driving intra-specific variation remain unclear. Here, utilizing wildtype murine embryonic stem cells (mESCs) derived from distinct genetic backgrounds, we discovered a polymorphic MMERGLN element capable of regulating H3K27ac enrichment, transcription and higher-order chromatin structure of neighboring loci. We demonstrated that this polymorphic element enhanced the neighboring Klhdc4 gene’s expression in cis, which in turn altered activity of downstream stress response genes. The results suggest that the polymorphic ERV-derived cis-regulatory element contribute to strain-specific phenotypes from particular stimuli. Moreover, we identified thousands of potential polymorphic ERVs in mESCs from both strains and illustrated their potential to regulate nearby histone modifications and transcription. Overall, our findings show the mechanism of how polymorphic ERVs can shape the epigenome and transcriptional networks that give rise to phenotypic divergence between individuals.
2021-09-22 | GSE165214 | GEO
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2018-12-18 | GSE123965 | GEO
Project description:see publication, arrays from 4 XXY genotypes containing polymorphic Y chromosomes
2010-10-02 | GSE23612 | GEO
Project description:We developed a novel approach combining next generation sequencing, bioinformatics and mass spectrometry to assess the impact of non-MHC polymorphisms on the repertoire of MHC I-associated peptides (MIPs). We compared the genomic landscape of MIPs eluted from B lymphoblasts of two MHC-identical siblings and determined that MIPs mirror the genomic frequency of non-synonymous polymorphisms but they behave as recessive traits at the surface level. Moreover, we showed that 11.7% of the MIP coding exome is polymorphic at the population level. Our method provides fundamental insights into the relation between the genomic self and the immune self and accelerates the discovery of polymorphic MIPs (also known as minor histocompatibility antigens), which play a major role in allo-immune responses. RNA-seq of human B lymphoblasts derived from peripheral blood mononuclear cells from 2 HLA-identical female siblings.
2013-12-08 | E-GEOD-48918 | biostudies-arrayexpress
Project description:Commensal bacteria influence host physiology, including immune responses, without invading host tissues. We show that proteins from segmented filamentous bacteria (SFB), which are immunomodulatory commensal microbes, are transferred into intestinal epithelial cells by adhesion-directed endocytosis that is distinct from the clathrin-dependent endocytosis of invasive pathogens. SFB transfer microbial cell wall-associated proteins, including an antigen that stimulates mucosal Th17 cell differentiation, into the cytosol of epithelial cells. Removal of CDC42 activity in vivo led to disruption of endocytosis induced by SFB, decreased epithelial antigen acquisition with consequent loss of immune modulation by SFB-specific CD4 T cells and mucosal Th17 cells. Our findings indicate direct communication between a resident gut microbe and the host and show that intestinal epithelial cells acquire antigens from commensal bacteria for generation of T-cell responses to the resident microbiota.
2019-01-10 | GSE124848 | GEO
Project description:see publication, arrays from 4 XXY genotypes containing polymorphic Y chromosomes Dye swaps, loop design.
2010-10-02 | E-GEOD-23612 | biostudies-arrayexpress