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Interleukin-13-mediated paneth cell degranulation and antimicrobial peptide release.

Authors
  • Stockinger, Silvia
  • Albers, Thorben
  • Duerr, Claudia U
  • Ménard, Sandrine
  • Pütsep, Katrin
  • Andersson, Mats
  • Hornef, Mathias W
Type
Published Article
Journal
Journal of Innate Immunity
Publisher
S. Karger AG
Publication Date
Jan 01, 2014
Volume
6
Issue
4
Pages
530–541
Identifiers
DOI: 10.1159/000357644
PMID: 24556597
Source
Medline
License
Unknown

Abstract

Paneth cell-derived enteric antimicrobial peptides significantly contribute to antibacterial host defense and host-microbial homeostasis. Regulation occurs by enzymatic processing and release into the small intestinal lumen, but the stimuli involved are incompletely understood. Here, the capacity of various microbial and immune stimuli to induce antimicrobial peptide release from small intestinal tissue was systematically evaluated using antibacterial activity testing, immunostaining for Paneth cell granules and mass spectrometry. We confirmed the stimulatory activity of the muscarinic receptor agonist carbachol and the nucleotide-binding oligomerization domain ligand muramyl dipeptide. In contrast, no release of antibacterial activity was noted after treatment with the Toll-like receptor ligands poly(I:C), lipopolysaccharide or CpG, and the cytokines interleukin (IL)-15, IL-22, IL-28 and interferon-γ. Rapid Paneth cell degranulation and antimicrobial activity release, however, was observed after stimulation with the endogenous mediators IL-4 and IL-13. This process required phosphatidylinositol 3-kinase and was associated with protein kinase B phosphorylation in Paneth cells. Flow cytometric analysis confirmed expression of the IL-13 receptor α1 on isolated Paneth cells. Our findings identify a novel role of IL-13 as inducer of Paneth cell degranulation and enteric antimicrobial peptide release. IL-13 may thus contribute to mucosal antimicrobial host defense and host microbial homeostasis.

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