| First Author | Gao R | Year | 2015 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 309 |
| Issue | 11 | Pages | L1376-81 |
| PubMed ID | 26453518 | Mgi Jnum | J:233217 |
| Mgi Id | MGI:5780960 | Doi | 10.1152/ajplung.00219.2015 |
| Citation | Gao R, et al. (2015) Deletion of Src family kinase Lyn aggravates endotoxin-induced lung inflammation. Am J Physiol Lung Cell Mol Physiol 309(11):L1376-81 |
| abstractText | 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 inflammatory 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 inflammation and proinflammatory signaling. We found increased activation of proinflammatory transcription factor NF-kappaB 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-1beta cleavage and activation. The aggravated lung inflammatory signaling in Lyn(-/-) mice was associated with increased production of proinflammatory 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 inflammation. |
