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Chlamydia trachomatis Requires Functional Host-Cell Mitochondria and NADPH Oxidase 4/p38MAPK Signaling for Growth in Normoxia

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Title: Chlamydia trachomatis Requires Functional Host-Cell Mitochondria and NADPH Oxidase 4/p38MAPK Signaling for Growth in Normoxia
Authors: Thapa, Jeewan Browse this author →KAKEN DB
Yoshiiri, Gen Browse this author
Ito, Koki Browse this author →KAKEN DB
Okubo, Torahiko Browse this author →KAKEN DB
Nakamura, Shinji Browse this author →KAKEN DB
Furuta, Yoshikazu Browse this author
Higashi, Hideaki Browse this author →KAKEN DB
Yamaguchi, Hiroyuki Browse this author →KAKEN DB
Keywords: Chlamydia trachomatis
NADPH oxidase
Issue Date: 26-May-2022
Publisher: Frontiers Media
Journal Title: Frontiers in Cellular and Infection Microbiology
Volume: 12
Start Page: 902492
Publisher DOI: 10.3389/fcimb.2022.902492
Abstract: Chlamydia trachomatis (Ct) is an intracellular energy-parasitic bacterium that requires ATP derived from infected cells for its growth. Meanwhile, depending on the O-2 concentration, the host cells change their mode of ATP production between oxidative phosphorylation in mitochondria (Mt) and glycolysis; this change depends on signaling via reactive oxygen species (ROS) produced by NADPH oxidases (NOXs) as well as Mt. It has been proposed that Ct correspondingly switches its source of acquisition of ATP between host-cell Mt and glycolysis, but this has not been verified experimentally. In the present study, we assessed the roles of host-cell NOXs and Mt in the intracellular growth of CtL2 (L2 434/Bu) under normoxia (21% O-2) and hypoxia (2% O-2) by using several inhibitors of NOXs (or the downstream molecule) and Mt-dysfunctional (Mt(d)) HEp-2 cells. Under normoxia, diphenyleneiodonium, an inhibitor of ROS diffusion, abolished the growth of CtL2 and other Chlamydiae (CtD and C. pneumoniae). Both ML171 (a pan-NOX inhibitor) and GLX351322 (a NOX4-specific inhibitor) impaired the growth of CtL2 under normoxia, but not hypoxia. NOX4-knockdown cells diminished the bacterial growth. SB203580, an inhibitor of the NOX4-downstream molecule p38MAPK, also inhibited the growth of CtL2 under normoxia but not hypoxia. Furthermore, CtL2 failed to grow in Mt(d) cells under normoxia, but no effect was observed under hypoxia. We conclude that under normoxia, Ct requires functional Mt in its host cells as an ATP source, and that this process requires NOX4/p38MAPK signaling in the host cells. In contrast to hypoxia, crosstalk between NOX4 and Mt via p38MAPK may be crucial for the growth of Ct under normoxia.
Type: article
Appears in Collections:人獣共通感染症国際共同研究所 (International Institute for Zoonosis Control) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

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