%0 Journal Article
%T cIAP-1 Controls Innate Immunity to C. pneumoniae Pulmonary Infection
%A Hridayesh Prakash
%A Daniel Becker
%A Linda B£¿hme
%A Lori Albert
%A Martin Witzenrath
%A Simone Rosseau
%A Thomas F. Meyer
%A Thomas Rudel
%J PLOS ONE
%D 2009
%I Public Library of Science (PLoS)
%R 10.1371/journal.pone.0006519
%X The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-¦Ã) was increased whereas that of Tumor Necrosis Factor (TNF-¦Á) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
%U http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0006519