Aussie Gut: Integrated gut microbial and mucosal inflammatory profiling in obesity — ASN Events

Aussie Gut: Integrated gut microbial and mucosal inflammatory profiling in obesity (#405)

Nicholas P West 1 , Amanda J Cox 1 , Ping Zhang 1 , Barbara Fazekas de St Groth 2 , Helen McGuire 2 , Chris McSweeney 3 , Jelena Vider 1 , Stuart Denman 3 , Benedict Devereaux 4 , Allan Cripps 5
  1. Medical Science, Griffith University, Parklands, QLD, Australia
  2. Ramaciotti Centre for Systems Biology, University of Sydney, Camperdown, NSW, Australia
  3. CSIRO, St Lucia, QLD, Australia
  4. Digestive Diseases Queensland, Chermside, QLD, Australia
  5. Department of Medicine, Griffith University, Parklands, Queensland, Australia

Changes in gut microbiota link obesity and chronic inflammation through mucosal inflammation (1). The aim of this study was to compare gut microbiota and mucosal and systemic inflammation in 16 healthy (BMI 24 ± 1.35 m/kg2, age 47 ± 11 y) and 16 obese individuals (BMI 31 ± 3.50 m/kg2, mean and SD, age 46 ± 7.5 y) without evidence of metabolic syndrome (MetS). A total of 32 individuals (50% female) undergoing colonoscopy were recruited, provided they were not taking immune modulating medications and had no evidence of histopathology. Participants provided a faecal and blood sample and biopsies from the ascending colon were collected during colonoscopy. Faecal microbial analysis was undertaken with 16s rRNA analysis. Peripheral blood mononuclear cells (PBMCs) and ascending colon lamina propria mononuclear cells (AC-LPMCs) were assessed by flow cytometry for quantitation of effector/memory (CD45RO+) and naive (CD45RO-) CD4+T cells, MAIT cells and T-regs while immune gene expression was assessed using the nCounter® PanCancer Immune Profiling panel (NanoString Technologies, WA, USA). Obese individuals had a significantly higher concentration of CRP, ESR, fasting blood glucose, and blood pressure. Based on the Shannon diversity index there was little difference in faecal microbial species richness or diversity between the groups (healthy group 3.78 ± 0.4 v obese group 3.66 ± 0.43; p=0.42). Partial least squares – discriminant analysis revealed distinct clustering of faecal microbial genera between the groups. The frequency of PBMC lymphocytes (CD3+ CD4-) expressing the natural killer cell marker (CD161hi) was significantly higher in obese individuals. The ratio of AC-LPMC T-regs to CD8+ T-cells and CD4+ T-cells to total T-cells from gene expression cell specific profiling separated obese from healthy individuals. Overall obesity without MetS was associated with altered systemic and mucosal inflammation, and an altered gut microbial composition.

  1. (1). A.J. Cox, N.P. West, A.W. Cripps, Obesity, inflammation, and the gut microbiota, The lancet. Diabetes & endocrinology 3(3) (2015) 207-15
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