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

Thapa, Jeewan; Yoshiiri, Gen; Ito, Koki; Okubo, Torahiko; Nakamura, Shinji; Furuta, Yoshikazu; Higashi, Hideaki; Yamaguchi, Hiroyuki

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

Thapa, Jeewan; Yoshiiri, Gen; Ito, Koki et al.

Frontiers in Cellular and Infection Microbiology, 2022, 12, 902492

Permalink : https://hdl.handle.net/2115/86360

このアイテムのアクセス数:568件（2026-08-14 21:28 集計）

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https://doi.org/10.3389/fcimb.2022.902492			8

論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/86360
タイトル	Chlamydia trachomatis Requires Functional Host-Cell Mitochondria and NADPH Oxidase 4/p38MAPK Signaling for Growth in Normoxia
著者	Thapa, Jeewan ; Yoshiiri, Gen ; Ito, Koki ; Okubo, Torahiko ; Nakamura, Shinji ; Furuta, Yoshikazu ; Higashi, Hideaki ; Yamaguchi, Hiroyuki
e-Rad_Researcher 40837449 著者名 Thapa, Jeewan
著者名 Yoshiiri, Gen
e-Rad_Researcher 40455663 著者名 Ito, Koki
e-Rad_Researcher 90762196 著者名 Okubo, Torahiko
e-Rad_Researcher 40207882 著者名 Nakamura, Shinji
著者名 Furuta, Yoshikazu
e-Rad_Researcher 20311227 著者名 Higashi, Hideaki
e-Rad_Researcher 40221650 著者名 Yamaguchi, Hiroyuki
言語	英語
キーワード	Chlamydia trachomatis
	mitochondria
	normoxia
	hypoxia
	NADPH oxidase
	NOX4
	p38MAPK
発行日	2022-05-26
出版者	Frontiers Media
収録物名	Frontiers in Cellular and Infection Microbiology
巻(号)	12
ページ	902492
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
PISSN	2235-2988
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.3389/fcimb.2022.902492