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    J Immunol. 2006 Mar 15;176(6):3813-20.

    Preprotachykinin-A gene products are key mediators of lung injury in polymicrobial sepsis.

    Puneet P, Hegde A, Ng SW, Lau HY, Lu J, Moochhala SM, Bhatia M.

    Source

    Department of Pharmacology, National University of Singapore, 18 Medical Drive, Singapore 117597.

    Abstract

    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.

    PMID:
    16517752
    [PubMed - indexed for MEDLINE]
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