TY - JOUR
T1 - Enhancement of reactive oxygen species production and chlamydial infection by the mitochondrial Nod-like family member NLRX1
AU - Abdul-Sater, Ali A.
AU - Saïd-Sadier, Najwane
AU - Lam, Verissa M.
AU - Singh, Bhavni
AU - Pettengill, Matthew A.
AU - Soares, Fraser
AU - Tattoli, Ivan
AU - Lipinski, Simone
AU - Girardin, Stephen E.
AU - Rosenstiel, Philip
AU - Ojcius, David M.
PY - 2010/12/31
Y1 - 2010/12/31
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=78650630756&partnerID=8YFLogxK
U2 - 10.1074/jbc.M110.137885
DO - 10.1074/jbc.M110.137885
M3 - 文章
C2 - 20959452
AN - SCOPUS:78650630756
SN - 0021-9258
VL - 285
SP - 41637
EP - 41645
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 53
ER -