| First Author | Puneet P | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 6 | Pages | 3813-20 |
| PubMed ID | 16517752 | Mgi Jnum | J:129532 |
| Mgi Id | MGI:3769623 | Doi | 10.4049/jimmunol.176.6.3813 |
| Citation | Puneet P, et al. (2006) Preprotachykinin-A gene products are key mediators of lung injury in polymicrobial sepsis. J Immunol 176(6):3813-20 |
| abstractText | Preprotachykinin-A (PPT-A) gene products substance P and neurokinin-A have been shown to play an important role in neurogenic inflammation. To investigate the role of PPT-A gene products in lung injury in sepsis, polymicrobial sepsis was induced by cecal ligation and puncture in PPT-A gene-deficient mice (PPT-A(-/-)) and the wild-type control mice (PPT-A(+/+)). PPT-A gene deletion significantly protected against mortality, delayed the onset of lethality, and improved the long-term survival following cecal ligation and puncture-induced sepsis. PPT-A(-/-) mice also had significantly attenuated inflammation and damage in the lungs. The data suggest that deletion of the PPT-A gene may have contributed to the disruption in recruitment of inflammatory cells resulting in protection against tissue damage, as in these mice the sepsis-associated increase in chemokine levels is significantly attenuated. |
