complement factor c7 contributes to lung immunopathology caused by mycobacterium tuberculosisc7补充因素导致肺癌免疫病理由结核分枝杆菌引起的.pdfVIP
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complement factor c7 contributes to lung immunopathology caused by mycobacterium tuberculosisc7补充因素导致肺癌免疫病理由结核分枝杆菌引起的
Hindawi Publishing Corporation
Clinical and Developmental Immunology
Volume 2012, Article ID 429675, 7 pages
doi:10.1155/2012/429675
Research Article
Complement Factor C7 Contributes to Lung Immunopathology
Caused by Mycobacterium tuberculosis
Kerry J. Welsh,1 Cole T. Lewis,1 Sydney Boyd,1 Michael C. Braun,2 and Jeffrey K. Actor1
1 Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, Houston, TX 77030, USA
2 Department of Pediatrics-Renal Section, Texas Children’s Hospital, Baylor College of Medicine, Houston, TX 77030, USA
Correspondence should be addressed to Jeffrey K. Actor, jeffrey.k.actor@
Received 11 May 2012; Accepted 20 July 2012
Academic Editor: Daniel Rittirsch
Copyright © 2012 Kerry J. Welsh et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Mycobacterium tuberculosis (MTB) remains a significant global health burden despite the availability of antimicrobial chemother-
apy. Increasing evidence indicates a critical role of the complement system in the development of host protection against the
bacillus, but few studies have specifically explored the function of the terminal complement factors. Mice deficient in complement
C7 and wild-type C57BL/6 mice were aerosol challenged with MTB Erdman and assessed for bacterial burden, histopathology, and
lung cytokine responses at days 30 and 60 post-infection. Macrophages isolated from C7 −/− and wild-type mice were evaluated for
MTB proliferation and cytokine production. C7 −/− mice had significantly less liver colony forming units (CFUs) at day 30; no
differences were noted in lung CFUs. The C7 deficient mice had markedly redu
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