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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Preprotachykinin-A gene products are key mediators of lung injury in polymicrobial sepsis. Puneet, P., Hegde, A., Ng, S.W., Lau, H.Y., Lu, J., Moochhala, S.M., Bhatia, M. J. Immunol. (2006) [Pubmed]
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