Chlamydia trachomatis-infected host cells resist dsRNA-induced apoptosis.
Cell Microbiol. 2010 Sep 1; 12(9):1340-51
This article PDF usually requires a subscription to access but you can receive the PDF, at no cost, through a special arrangement between Springer Science+Business Media and Faculty of 1000 for our Faculty Members who act as reviewers. This PDF is provided to you only for the purposes of reviewing the article while you consider preparing a recommendation of the article for F1000Prime. Other than for this purpose you warrant that you will treat the PDF as confidential. Furthermore you warrant that you will not use the PDF for any other purpose, especially but not limited to forwarding, copying, selling, distributing it whether commercially or non-commercially and that you will not make it available on any website for any other purpose.
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, 30 Jan 2015; F1000Prime.com/5397956
Get the most out of F1000Prime - attend a live online demonstration.
Please choose one of the following time zones:
Want to become an
has been added to your "Faculty I'm Following" page in MyF1000
Follow/Unfollow any Faculty via their recommendations, biography pages, or MyF1000
If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password.
The email address should be the one you originally registered with F1000.
You registered with F1000 via Google, so we cannot reset your password.
To sign in, please click here.
If you still need help with your Google account password, please click here.
You registered with F1000 via Facebook, so we cannot reset your password.
To sign in, please click here.
If you still need help with your Facebook account password, please click here.
We have sent an email to , please follow the instructions to reset your password.
If you don't receive this email, please check your spam filters and/or contact email@example.com.