ORCiD
David M. Ojcius: 0000-0003-1461-4495
Department
Biomedical Sciences
Document Type
Article
Publication Title
Journal of Biological Chemistry
ISSN
0021-9258
Volume
285
Issue
53
DOI
10.1074/jbc.M110.137885
First Page
41637
Last Page
41645
Publication Date
12-31-2010
Abstract
Chlamydia trachomatis infections cause severe and irreversible damage that can lead to infertility and blindness in both males and females. Following infection of epithelial cells, Chlamydia induces production of reactive oxygen species (ROS). Unconventionally, Chlamydiae use ROS to their advantage by activating caspase-1, which contributes to chlamydial growth. NLRX1, a member of the Nod-like receptor family that translocates to the mitochondria, can augment ROS production from the mitochondria following Shigella flexneri infections. However, in general, ROS can also be produced by membrane-bound NADPH oxidases. Given the importance of ROS-induced caspase-1 activation in growth of the chlamydial vacuole, we investigated the sources of ROS production in epithelial cells following infection with C. trachomatis. In this study, we provide evidence that basal levels of ROS are generated during chlamydial infection by NADPH oxidase, but ROS levels, regardless of their source, are enhanced by an NLRX1-dependent mechanism. Significantly, the presence of NLRX1 is required for optimal chlamydial growth.
Recommended Citation
Abdul-Sater, A. A.,
Saïd-Sadier, N.,
Lam, V. M.,
Singh, B.,
Pettengill, M. A.,
Soares, F.,
Tattoli, I.,
Lipinski, S.,
Girardin, S. E.,
Rosenstiel, P.,
&
Ojcius, D. M.
(2010).
Enhancement of reactive oxygen species production and chlamydial infection by the mitochondrial Nod-like family member NLRX1.
Journal of Biological Chemistry, 285(53), 41637–41645.
DOI: 10.1074/jbc.M110.137885
https://scholarlycommons.pacific.edu/dugoni-facarticles/30
Included in
Biochemistry Commons, Immunity Commons, Immunology of Infectious Disease Commons, Medical Immunology Commons
