Unknown,Transcriptomics,Genomics,Proteomics

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Gender bias in autoimmunity is influenced by microbiota

ABSTRACT: Gender bias and the role of sex hormones in autoimmune diseases are well established. In specific-pathogen free (SPF) non-obese diabetic (NOD) mice females have 1.3-4.4 times higher incidence of Type 1 diabetes (T1D). Germ-free (GF) mice lose the gender bias (female/male ratio 1.1-1.2). Gut microbiota differed in males and females, a trend reversed by male castration, confirming that androgens influence gut microbiota. Colonization of GF NOD mice with defined microbiota revealed that some but not all lineages overrepresented in male mice supported a gender bias in T1D, and protection did not correlate with androgen levels. However, hormone-supported selective microbial lineage variation may work as a positive feedback mechanism contributing to the sexual dimorphism of autoimmune diseases. Gene expression analysis suggested pathways involved in protection of males from T1D by microbiota. We compared gene expression patterns in the pancreatic lymph nodes (PLNs) between four groups of mice (two genders in SPF and GF conditions, respectively). PLNs were isolated from 9-10 week old GF and SPF male and female NOD mice with 3 mice in each group, for a total of 12 samples.

ORGANISM(S): Mus musculus

SUBMITTER: Aly Khan

PROVIDER: E-GEOD-49467 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Introduction: Diagnosis of severe influenza pneumonia remains challenging because of the lack of correlation between presence of influenza virus and patient’s clinical status. We conducted gene expression profiling in the whole blood of critically ill patients to identify a gene signature that would allow clinicians to distinguish influenza infection from other causes of severe respiratory failure (e.g. bacterial pneumonia, non-infective systemic inflammatory response syndrome). Methods: Whole blood samples were collected from critically ill individuals and assayed on Illumina HT-12 gene expression beadarrays. Differentially expressed genes were determined by linear mixed model analysis and over-represented biological pathways determined using GeneGo MetaCore. Results: The gene expression profile of H1N1 influenza A pneumonia was distinctly different from bacterial pneumonia and systemic inflammatory response syndrome. The influenza gene expression profile is characterized by up-regulation of genes from cell cycle regulation, apoptosis and DNA-damage response pathways. In contrast, no distinctive gene-expression signature was found in patients with bacterial pneumonia or systemic inflammatory response syndrome. The gene expression profile of influenza infection persisted through five days of follow-up. Furthermore, in patients with primary H1N1 influenza A infection who subsequently developed bacterial co-infection, the influenza gene-expression signature remained unaltered, despite the presence of a super-imposed bacterial infection. Conclusions: The whole blood expression profiling data indicates that the host response to influenza pneumonia is distinctly different from that caused by bacterial pathogens. This information may speed up identification of the cause of infection in patients presenting with severe respiratory failure, allowing appropriate patient care to be undertaken more rapidly. Daily PAXgene samples for up to 5 days for; influenza A pneumonia patients (n=8), bacterial pneumonia patients (n=16), mixed bacterial and influenza A pneumonia patients (n=3), systemic inflammatory response patients (SIRS, n=13). Days 1 and 5 PAXgene samples for healthy control individuals

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Gender bias in autoimmunity is influenced by microbiota

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