Open AccessNF‐κB and inhibitor of apoptosis proteins are required for apoptosis resistance of epithelial cells persistently infected with Chlamydophila pneumoniae
Author(s) -
Paland Nicole,
Rajalingam Krishnaraj,
Machuy Nikolaus,
Szczepek Agnes,
Wehrl Wolfgang,
Rudel Thomas
Publication year - 2006
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2006.00739.x
Subject(s) - inhibitor of apoptosis , apoptosis , staurosporine , biology , chlamydophila pneumoniae , gene silencing , inhibitor of apoptosis domain , downregulation and upregulation , tumor necrosis factor alpha , nf κb , nfkb1 , programmed cell death , microbiology and biotechnology , cancer research , signal transduction , immunology , chlamydiaceae , protein kinase c , antibody , transcription factor , caspase , gene , biochemistry
Summary Infection with Chlamydophila pneumoniae (Cpn) renders host cells resistant to apoptosis induced by a variety of stimuli. While modulation of apoptosis has been extensively studied in cells acutely infected with Cpn, very little is known on how persistent chlamydial infection influences host cell survival. Here we show that epithelial cells persistently infected with Cpn resist apoptosis induced with TNFα or staurosporine. Cpn induced the activation of nuclear factor kappa B (NF‐κB) and inhibition of NF‐κB with a chemical inhibitor or by silencing expression of the p65 subunit sensitized infected cells for apoptosis induction by staurosporine or TNFα. Persistent infection resulted in the upregulation of the NF‐κB regulated inhibitor of apoptosis protein 2 (cIAP‐2) but not inhibitor of apoptosis protein 1 (cIAP‐1). Interestingly, silencing of either cIAP‐1 or cIAP‐2 sensitized infected cells, suggesting that IAPs play an important role in the apoptosis resistance of persistently infected cells.