| First Author | Koike Y | Year | 2012 |
| Journal | Immunol Lett | Volume | 148 |
| Issue | 2 | Pages | 172-7 |
| PubMed ID | 23022387 | Mgi Jnum | J:319020 |
| Mgi Id | MGI:6862369 | Doi | 10.1016/j.imlet.2012.08.008 |
| Citation | Koike Y, et al. (2012) MyD88-dependent interleukin-10 production from regulatory CD11b(+)Gr-1(high) cells suppresses development of acute cerulein pancreatitis in mice. Immunol Lett 148(2):172-7 |
| abstractText | 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-1(high) 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. |
