Open AccessToll‐like receptors 2 and 4 modulate intestinal IL‐10 differently in ileum and colon
Author(s) -
Latorre Eva,
Layunta Elena,
Grasa Laura,
Pardo Julián,
García Santiago,
Alcalde Ana I,
Mesonero José E
Publication year - 2018
Publication title -
ueg journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.667
H-Index - 35
eISSN - 2050-6414
pISSN - 2050-6406
DOI - 10.1177/2050640617727180
Subject(s) - tlr2 , tlr4 , toll like receptor , intestinal epithelium , enterocyte , ileum , immune system , receptor , innate immune system , intestinal mucosa , cytokine , immunology , medicine , epithelium , biology , microbiology and biotechnology , small intestine , pathology
Background Inflammatory bowel diseases are consequence of an intestinal homeostasis breakdown in which innate immune dysregulation is implicated. Toll‐like receptor (TLR)2 and TLR4 are immune recognition receptors expressed in the intestinal epithelium, the first physical‐physiological barrier for microorganisms, to inform the host of the presence of Gram‐positive and Gram‐negative organisms. Interleukin (IL)‐10 is an essential anti‐inflammatory cytokine that contributes to maintenance of intestinal homeostasis. Aim Our main aim was to investigate intestinal IL‐10 synthesis and release, and whether TLR2 and TLR4 are determinants of IL‐10 expression in the intestinal tract. Methods We used Caco‐2 cell line as an enterocyte‐like cell model, and also ileum and colon from mice deficient in TLR2, TLR4 or TLR2/4 to test the involvement of TLR signaling. Results Intestinal epithelial cells are able to synthesize and release IL‐10 and their expression is increased after TLR2 or TLR4 activation. IL‐10 regulation seems to be tissue specific, with IL‐10 expression in the ileum regulated by a compensation between TLR2 and TLR4 expression, whereas in the colon, TLR2 and TLR4 affect IL‐10 expression independently. Conclusions Intestinal epithelial cells could release IL‐10 in response to TLR activation, playing an intestinal tissue‐dependent and critical intestinal immune role.