Chlamydia trachomatis-infected host cells resist dsRNA-induced apoptosis.
Cell Microbiol. 2010 Sep 1; 12(9):1340-51
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Böhme et al. describe a novel anti-apoptotic mechanism in Chlamydia-infected cells. These cells are resistant to dsRNA-induced apoptosis, which is dependent on the caspase-8 modulator cFlip.
Apoptosis is a form of programmed cell death that is an essential component of the innate immune system so as to prevent the spread of infection. Several pathogens have evolved mechanisms to manipulate this host cell defense in order to survive and replicate. Obligate intracellular pathogens such as Chlamydia spp. have developed anti-apoptotic strategies to be able to colonize host cells, leading to chronic infection. Several studies have shown that Chlamydia-infected cells are resistant to several forms of apoptosis upstream of the mitochondria. In this paper, the authors describe a novel anti-apoptotic mechanism in which Chlamydia trachomatis-infected cells are resistant to dsRNA. Utilizing synthetic dsRNA (polyl:C) that mimics viral infections, Böhme et al. clearly show that Chlamydia-infected cells have decreased caspase-8, caspase-9 and caspase-3 cleavage products, as well as decreased caspase activity. Surprisingly, treatment of Chlamydia-infected cells with tumor necrosis factor (TNF)-alpha led to caspase-8 activation. This result suggested that C. trachomatis blocks apoptosis, with distinct mechanisms depending on the stimuli. Previous studies indicated that polyl:C induces apoptosis through the dsRNA-dependent protein kinase (PKR) leading to caspase-8 activation. The initial hypothesis by Böhme et al. was that Chlamydia directly inhibited PKR, leading to apoptotic resistance. However, both PKR and eIF2-alpha were still activated in Chlamydia-infected cells. Upon further investigation, this group found that cFlip, a modulator of caspase-8, is necessary for the prevention of dsRNA-dependent apoptosis. The exact mechanism by which Chlamydia interferes with cFlip remains unknown; however, the authors suggest that an unidentified Chlamydia effector protein affects local cFlip activity, which prevents dsRNA-dependent apoptosis.
Brumell J and Brabant D: F1000Prime Recommendation of [Böhme L et al., Cell Microbiol 2010, 12(9):1340-51]. In F1000Prime, 13 Oct 2010; DOI: 10.3410/f.5397956.5431066. F1000Prime.com/5397956#eval5431066
F1000Prime Recommendations, Dissents and Comments for [Böhme L et al., Cell Microbiol 2010, 12(9):1340-51]. In F1000Prime, 31 Oct 2014; F1000Prime.com/5397956
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