Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells

Published on 2017-09-12T17:41:05Z (GMT) by
<div><p>Interleukin 33 (IL-33), an inflammatory and mechanically responsive cytokine, is an important component of a TLR4-dependent innate immune process in mucosal epithelium. Although TLR4 also plays a role in sensing biomechanical stretch, a pathway of stretch-induced TLR4-dependent IL-33 biosynthesis has not been revealed. In the current study, we show that short term (6 h) cyclic stretch (CS) of cultured murine respiratory epithelial cells (MLE-12) increased intracellular IL-33 expression in a TLR4 dependent fashion. There was no detectable IL-33 in conditioned media in this interval. CS, however, increased release of the notable alarmin, HMGB1, and a neutralizing antibody (2G7) to HMGB1 completely abolished the CS mediated increase in IL-33. rHMGB1 increased IL-33 synthesis and this was partially abrogated by silencing TLR4 suggesting additional receptors for HMGB1 are involved in its regulation of IL-33. Collectively, these data reveal a HMGB1/TLR4/IL-33 pathway in the response of respiratory epithelium to mechanical stretch.</p></div>

Cite this collection

Chang, Jing; Xia, Yuefeng; Wasserloos, Karla; Deng, Meihong; Blose, Kory J.; Vorp, David A.; Turnquist, Heth R.; R. Billiar, Timothy; Pitt, Bruce A.; Zhang, Ma-Zhong; Zhang, Li-Ming (2017): Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells. PLOS ONE.

https://doi.org/10.1371/journal.pone.0184770

Retrieved: 02:28, Nov 18, 2017 (GMT)