Involvement of Skeletal Muscle Gene Regulatory Network in Susceptibility to Wound Infection Following Trauma

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Involvement of Skeletal Muscle Gene Regulatory Network in Susceptibility to Wound Infection Following Trauma

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Title: Involvement of Skeletal Muscle Gene Regulatory Network in Susceptibility to Wound Infection Following Trauma
Author: Apidianakis, Yiorgos; Mindrinos, Michael N.; Xiao, Wenzhong; Tegos, George; Papisov, Mikhail Ivanovich; Hamblin, Michael; Davis, Ronald W.; Tompkins, Ronald Gary; Rahme, Laurence G.

Note: Order does not necessarily reflect citation order of authors.

Citation: Apidianakis, Yiorgos, Michael N. Mindrinos, Wenzhong Xiao, George P. Tegos, Michail I. Papisov, Michael R. Hamblin, Ronald W. Davis, Ronald G. Tompkins, and Laurence G. Rahme. 2007. Involvement of skeletal muscle gene regulatory network in susceptibility to wound infection following trauma. PLoS ONE 2(12): e1356.
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Abstract: Despite recent advances in our understanding the pathophysiology of trauma, the basis of the predisposition of trauma patients to infection remains unclear. A Drosophila melanogaster/Pseudomonas aeruginosa injury and infection model was used to identify host genetic components that contribute to the hyper-susceptibility to infection that follows severe trauma. We show that P. aeruginosa compromises skeletal muscle gene (SMG) expression at the injury site to promote infection. We demonstrate that activation of SMG structural components is under the control of cJun-N-terminal Kinase (JNK) Kinase, Hemipterous (Hep), and activation of this pathway promotes local resistance to P. aeruginosa in flies and mice. Our study links SMG expression and function to increased susceptibility to infection, and suggests that P. aeruginosa affects SMG homeostasis locally by restricting SMG expression in injured skeletal muscle tissue. Local potentiation of these host responses, and/or inhibition of their suppression by virulent P. aeruginosa cells, could lead to novel therapies that prevent or treat deleterious and potentially fatal infections in severely injured individuals.
Published Version: doi://10.1371/journal.pone.0001356
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2131783/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10024351

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