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Dysregulation of the colonic mucosally-adherent microbiota associates with HIV disease progression.

ABSTRACT: HIV is known to severely affect the gastrointestinal immune system, in particular compartments of immunity that regulate gut microbial composition. Furthermore, recent studies in mice have shown that dysregulation of the gut microbiome can contribute to chronic inflammation, which is a hallmark of HIV and is thought to fuel disease progression. We sought to understand whether the gut microbial community differs in HIV-infected subjects, and whether such putative differences are associated with disease progression. We found that dysbiosis in the gut mucosally-adherent bacterial community associates with markers of chronic inflammation and disease progression in HIV-infected subjects, and this dysbiosis remains in many subjects undergiong antiretroviral therapy.

ORGANISM(S): Archaea Homo sapiens Bacteria

PROVIDER: GSE43746 | GEO | 2013/07/10

SECONDARY ACCESSION(S): PRJNA187524

REPOSITORIES: GEO

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Dysregulation of the colonic mucosally-adherent microbiota associates with HIV disease progression.

Project description:HIV is known to severely affect the gastrointestinal immune system, in particular compartments of immunity that regulate gut microbial composition. Furthermore, recent studies in mice have shown that dysregulation of the gut microbiome can contribute to chronic inflammation, which is a hallmark of HIV and is thought to fuel disease progression. We sought to understand whether the gut microbial community differs in HIV-infected subjects, and whether such putative differences are associated with disease progression. We found that dysbiosis in the gut mucosally-adherent bacterial community associates with markers of chronic inflammation and disease progression in HIV-infected subjects, and this dysbiosis remains in many subjects undergiong antiretroviral therapy. We used G3 PhyloChip microarrays (commercially available from Second Genome, Inc.) to profile gut bacteria in rectosigmoid biopsies from 32 subjects: 6 HIV-infected viremic untreated (VU), 18 HIV-infected subjects on highly active antiretroviral therapy (HAART), 1 HIV-infected long-term non-progressor that is untreated (LTNP), and 9 HIV-uninfected subjects (HIV-).

2013-07-10 | E-GEOD-43746 | biostudies-arrayexpress

Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.

2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress

Imbalanced gut microbiota drives nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in a fast-food diet mouse model

Project description:This study employed low and high-fat purified diets containing two levels of added dietary cholesterol in conventionally raised, specific-pathogen free (SPF) mice harboring a full microbial community as compared to germ-free (GF) mice raised in complete absence of gut microbes on disease outcomes. It was hypothesized that FF-diets would lead to an earlier onset of gut dysbiosis, corresponding with elevated biomarkers of NAFLD and NASH. In the present study, we aimed to dissect the role of FF diet induced gut dysbiosis in order to mechanistically identify the underlying mechanism that influences gut-liver crosstalk between specific diet-induced bacterial populations and hepatic tissue to drive NAFLD/NASH onset and progression

2023-04-27 | GSE190982 | GEO

Experimental Autoimmune Encephalomyelitis is Associated with Changes of the Microbiota Composition in the Gastrointestinal Tract

Project description:The gut microbiome is known to be sensitive to changes in the immune system, especially during autoimmune diseases such as Multiple Sclerosis (MS). Our study examines the changes to the gut microbiome that occur during Experimental Autoimmune Encephalomyelitis (EAE), an animal model for MS. We collected fecal samples at key stages of EAE progression and quantified microbial abundances with 16S V4 amplicon sequencing. Our analysis of the data suggests that commensal Lactobacillaceae fall in abundance during EAE while other commensal populations belonging to the Clostridiaceae, Ruminococcaceae, and Peptostreptococcaceae families expand. Community analysis with microbial co-occurrence networks points to these three taxa as mediators of gut microbiome dysbiosis. We also employed PICRUSt2 to impute MetaCyc Enzyme Consortium (EC) pathway abundances from the original microbial abundance data. From this analysis, we found that a number of imputed EC pathways responsible for the production of compounds with indole groups are enriched in mice undergoing EAE. Our analysis and interpretation of results provides a detailed picture of the changes to the gut microbiome that are occurring throughout the course of EAE disease progression.

2020-09-15 | GSE153118 | GEO

Strongyloides stercoralis infection reduces bacteria producing short-chain fatty acids and increases bacterial amino-acid biosynthesis in early CKD patients

Project description:Controlling the progression of chronic kidney disease (CKD) at an early stage is critical for reducing disease severity. A cross-sectional study of chronic kidney disease (CKD) patients at all stages with S. stercoralis infection found that helminth infection caused gut dysbiosis, which may be involved in CKD progression. Because of the variation of gut microbiome results with helminth infection, the cross-sectional study of 16S rRNA sequencing, therefore, is insufficient to draw valid conclusions and correct the effects of S. stercoralis on the early stages of CKD. Combination with other omics approach is warrant to be better understand the disease.

2024-01-24 | PXD039656 | JPOST Repository

NOD2-dependent licensing of the microbiota predispose to transmissible inflammation and tumorigenesis in the colon.

Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as Crohn’s disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation.

2013-01-02 | GSE32421 | GEO

Salivary cytokine alterations in HIV infection part 1

2011-09-09 | GSE24037 | GEO

Salivary cytokine alterations in HIV infection part 1

Project description:Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis. A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact.

2011-09-08 | E-GEOD-24037 | biostudies-arrayexpress

Salivary cytokine alterations in HIV infection part 2

Project description:A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A 40 cytokine custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact. Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis.

2011-09-08 | E-GEOD-24064 | biostudies-arrayexpress

Proinflammatory isoforms of IL-32 as novel and robust biomarkers for control failure in HIV-infected slow-progressors.

Project description:HIV-infected slow-progressors (SP) represent a heterogeneous group of subjects who spontaneously control HIV infection without treatment for several years while showing moderate signs of disease progression. Here we determined the frequency of SP subjects who showed loss of HIV control within our Canadian Cohort of HIV+ Slow-Progressors and identified the proinflammatory cytokine IL-32 as a robust biomarker for control failure.

2015-12-31 | GSE74790 | GEO

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