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Epithelial-microbial crosstalk in polymeric Ig receptor deficient mice
Dag Henrik Reikvam1, Muriel Derrien, Rejoanoul Islam
1Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital - Rikshospitalet, Oslo, Norway.
European Journal of Immunology
|August 7, 2012
Summary
The polymeric Ig receptor (pIgR) is crucial for maintaining gut microbiota stability and immune defense. Its absence in mice disrupts gut homeostasis, leading to increased susceptibility to colitis.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Innate and adaptive immunity maintain gut homeostasis with the microbiota.
- Polymeric Ig receptor (pIgR) transports dimeric IgA and pentameric IgM across the intestinal epithelium.
- Antibodies mediated by pIgR are key to intestinal mucosal immune defense.
Purpose of the Study:
- To investigate the role of pIgR in maintaining gut homeostasis and its impact on the gut microbiota.
- To determine the effect of pIgR deficiency on the host's susceptibility to inflammatory conditions like colitis.
Main Methods:
- Gene expression profiling of colonic epithelial cells from pIgR knockout (KO) and wild-type (WT) mice.
- 16S rRNA gene sequencing for microbial community analysis.
- Assessment of dextran sulfate sodium (DSS)-induced colitis in pIgR KO and WT mice.
Main Results:
- pIgR KO mice exhibited differential expression of over 200 genes in colonic epithelial cells compared to WT mice.
- Upregulation of antimicrobial peptides in pIgR KO mice occurred in a commensal-dependent manner.
- pIgR deficiency led to altered gut microbiota composition and increased susceptibility to DSS-induced colitis.
Conclusions:
- pIgR is essential for the stability of the commensal gut microbiota.
- Disruption of pIgR function compromises gut homeostasis and exacerbates colitis.
- The absence of pIgR significantly worsens the outcome of experimental colitis, highlighting its critical role in mucosal immunity.

