Deletion of src family kinase Lyn aggravates endotoxin-induced lung inflammation

Rong Gao, Zhongsen Ma, Mengshi Ma, Jinyan Yu, Jiao Chen, Zhenyu Li, Sreerama Shetty, Jian Fu

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Overwhelming acute inflammation often leads to tissue damage during endotoxemia. In the present study, we investigated the role of Lyn, a member of the Src family tyrosine kinases, in modulating inlammatory responses in a murine model of endotoxemia. We examined lung inflammatory signaling in Lyn knockout (Lyn-/-) mice and wild-type littermates (Lyn+/+) during endotoxemia. Our data indicate that Lyn deletion aggravates endotoxin-induced pulmonary inlammation and proin-lammatory signaling. We found increased activation of proinlam-matory transcription factor NF-ΚB in the lung tissues of Lyn-/- mice after endotoxin challenge. Furthermore, during endotoxemia, the lung tissues of Lyn-/- mice showed increased inflammasome activation indicated by augmented caspase-1 and IL-1ß cleavage and activation. The aggravated lung inflammatory signaling in Lyn-/- mice was associated with increased production of proinlammatory mediators and elevated matrix metallopeptidase 9 and reduced VE-cadherin levels. Our results suggest that Lyn kinase modulates inhibitory signaling to suppress endotoxin-induced lung inlammation.

Original languageEnglish
Pages (from-to)L1376-L1381
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number11
StatePublished - 2015

Bibliographical note

Publisher Copyright:
© 2015 the American Physiological Society.


  • Inlammasome
  • Inlammation
  • Kinase
  • Lung
  • Lyn

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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