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10.1371/journal.pone.0184770

http://scihub22266oqcxt.onion/10.1371/journal.pone.0184770
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suck abstract from ncbi


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pmid28898270
      PLoS+One 2017 ; 12 (9 ): e0184770
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  • Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells #MMPMID28898270
  • Chang J ; Xia Y ; Wasserloos K ; Deng M ; Blose KJ ; Vorp DA ; Turnquist HR ; Billiar TR ; Pitt BA ; Zhang MZ ; Zhang LM
  • PLoS One 2017[]; 12 (9 ): e0184770 PMID28898270 show ga
  • 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.
  • |*Mechanotransduction, Cellular [MESH]
  • |Animals [MESH]
  • |Cell Line [MESH]
  • |HMGB1 Protein/*metabolism [MESH]
  • |Interleukin-33/genetics/*metabolism [MESH]
  • |Mice [MESH]
  • |Respiratory Mucosa/*metabolism [MESH]
  • |Second Messenger Systems [MESH]
  • |Stress, Mechanical [MESH]


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