Preprotachykinin-A Gene Products Are Key Mediators of Lung Injury in Polymicrobial Sepsis | Zendy

Padmam Puneet | Zendy; Akhil Hegde | Zendy; Siaw Wei Ng | Zendy; Hon Yen Lau | Zendy; Lu Jia | Zendy; Shabbir Moochhala | Zendy; Madhav Bhatia | Zendy

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Preprotachykinin-A Gene Products Are Key Mediators of Lung Injury in Polymicrobial Sepsis

Author(s) -

Padmam Puneet,

Akhil Hegde,

Siaw Wei Ng,

Hon Yen Lau,

Lu Jia,

Shabbir Moochhala,

Madhav Bhatia

Publication year - 2006

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.176.6.3813

Subject(s) - key (lock) , sepsis , medicine , lung , microbiology and biotechnology , biology , immunology , ecology

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.

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