MyD88-dependent interleukin-10 production from regulatory CD11b+Gr-1high cells suppresses development of acute cerulein pancreatitis in mice

Yuji Koike, Takanori Kanai, Keita Saeki, Yuji Nakamura, Masaru Nakano, Yohei Mikami, Yoshiyuki Yamagishi, Nobuhiro Nakamoto, Hirotoshi Ebinuma, Toshifumi Hibi

研究成果: Article査読

9 被引用数 (Scopus)

抄録

We explored the role of the MyD88 signaling pathway. This pathway mediates the recognition of pathogen-associated molecular patterns and damage-associated molecular patterns via Toll-like receptors (TLRs) and/or IL-1/IL-18 via each cytokine receptor in a murine model of acute pancreatitis induced by cerulein administration. Our analysis revealed that: various TLRs and MyD88 molecules were constitutively expressed in the pancreas of cerulein-treated and untreated wild-type (WT) mice. MyD88-/- mice administered cerulein developed severe pancreatitis as compared with MyD88+/+ WT mice. The number of IL-10-expressing CD11b+Gr-1high cells in cerulein-administered MyD88-/- mice was significantly decreased. This was in accordance with a reciprocal increase in the infiltration of CD4+ T cells as compared with that in control MyD88+/+ mice. WT mice pretreated with antibiotics and administered cerulein developed milder pancreatitis as compared with control cerulein-administered mice without antibiotic treatment. The MyD88 signaling pathway contributes to the induction of regulatory IL-10-producing macrophages/myeloid-derived suppressor cells, possibly in response to non-bacterial components in the damaged pancreas. These results provide a new concept for therapeutic strategies against acute pancreatitis.

本文言語English
ページ(範囲)172-177
ページ数6
ジャーナルImmunology Letters
148
2
DOI
出版ステータスPublished - 2012 12 7

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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