IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy

Interleukin (IL)-25 is a cytokine released by airway epithelial cells responding to pathogens. Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo sel...

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Veröffentlicht in:International journal of molecular sciences 2021-12, Vol.23 (1), p.3
Hauptverfasser: Tsai, Mei-Lan, Tsai, Yi-Giien, Lin, Yu-Chih, Hsu, Ya-Ling, Chen, Yi-Ting, Tsai, Ming-Kai, Liao, Wei-Ting, Lin, Yi-Ching, Hung, Chih-Hsing
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container_title International journal of molecular sciences
container_volume 23
creator Tsai, Mei-Lan
Tsai, Yi-Giien
Lin, Yu-Chih
Hsu, Ya-Ling
Chen, Yi-Ting
Tsai, Ming-Kai
Liao, Wei-Ting
Lin, Yi-Ching
Hung, Chih-Hsing
description Interleukin (IL)-25 is a cytokine released by airway epithelial cells responding to pathogens. Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo selective degradation, known as mitophagy. In this study, we examined the effects of IL-25 on ROS production and mitophagy and investigated the underlying mechanisms. The human monocyte cell line was pretreated with IL-25 at different time points. ROS production was measured by flow cytometry. The involvement of mitochondrial activity in the effects of IL-25 on ROS production and subsequent mitophagy was evaluated by enzyme-linked immunosorbent assay, Western blotting, and confocal microscopy. IL-25 stimulation alone induced ROS production and was suppressed by N-acetylcysteine, vitamin C, antimycin A, and MitoTEMPO. The activity of mitochondrial complex I and complex II/III and the levels of p-AMPK and the mitophagy-related proteins were increased by IL-25 stimulation. The CCL-22 secretion was increased by IL-25 stimulation and suppressed by mitophagy inhibitor treatment and PINK1 knockdown. The Th2-like cytokine IL-25 can induce ROS production, increase mitochondrial respiratory chain complex activity, subsequently activate AMPK, and induce mitophagy to stimulate M2 macrophage polarization in monocytes.
doi_str_mv 10.3390/ijms23010003
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Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo selective degradation, known as mitophagy. In this study, we examined the effects of IL-25 on ROS production and mitophagy and investigated the underlying mechanisms. The human monocyte cell line was pretreated with IL-25 at different time points. ROS production was measured by flow cytometry. The involvement of mitochondrial activity in the effects of IL-25 on ROS production and subsequent mitophagy was evaluated by enzyme-linked immunosorbent assay, Western blotting, and confocal microscopy. IL-25 stimulation alone induced ROS production and was suppressed by N-acetylcysteine, vitamin C, antimycin A, and MitoTEMPO. The activity of mitochondrial complex I and complex II/III and the levels of p-AMPK and the mitophagy-related proteins were increased by IL-25 stimulation. The CCL-22 secretion was increased by IL-25 stimulation and suppressed by mitophagy inhibitor treatment and PINK1 knockdown. The Th2-like cytokine IL-25 can induce ROS production, increase mitochondrial respiratory chain complex activity, subsequently activate AMPK, and induce mitophagy to stimulate M2 macrophage polarization in monocytes.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23010003</identifier><identifier>PMID: 35008429</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acetylcysteine ; Acetylcysteine - pharmacology ; AMP-Activated Protein Kinases - metabolism ; Antimycin A - pharmacology ; Ascorbic acid ; Ascorbic Acid - pharmacology ; Asthma ; Autophagy ; Cell Polarity ; Chronic illnesses ; Confocal microscopy ; Cytokines ; Electron transport chain ; Enzyme-linked immunosorbent assay ; Epithelial cells ; Epithelium ; Flow Cytometry ; Humans ; Interleukin-17 - metabolism ; Interleukin-17 - pharmacology ; Kinases ; Lymphocytes T ; Macrophages ; Macrophages - cytology ; Macrophages - metabolism ; Microscopy, Confocal ; Mitochondria ; Mitochondria - metabolism ; Mitophagy ; Monocytes ; Monocytes - cytology ; Monocytes - metabolism ; NADH-ubiquinone oxidoreductase ; Organophosphorus Compounds - pharmacology ; Oxidative stress ; Phosphorylation - drug effects ; Piperidines - pharmacology ; Polarization ; Proteins ; PTEN-induced putative kinase ; Pulmonary fibrosis ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Respiratory tract ; Respiratory tract diseases ; Stimulation ; THP-1 Cells ; Western blotting</subject><ispartof>International journal of molecular sciences, 2021-12, Vol.23 (1), p.3</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo selective degradation, known as mitophagy. In this study, we examined the effects of IL-25 on ROS production and mitophagy and investigated the underlying mechanisms. The human monocyte cell line was pretreated with IL-25 at different time points. ROS production was measured by flow cytometry. The involvement of mitochondrial activity in the effects of IL-25 on ROS production and subsequent mitophagy was evaluated by enzyme-linked immunosorbent assay, Western blotting, and confocal microscopy. IL-25 stimulation alone induced ROS production and was suppressed by N-acetylcysteine, vitamin C, antimycin A, and MitoTEMPO. The activity of mitochondrial complex I and complex II/III and the levels of p-AMPK and the mitophagy-related proteins were increased by IL-25 stimulation. 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subjects Acetylcysteine
Acetylcysteine - pharmacology
AMP-Activated Protein Kinases - metabolism
Antimycin A - pharmacology
Ascorbic acid
Ascorbic Acid - pharmacology
Asthma
Autophagy
Cell Polarity
Chronic illnesses
Confocal microscopy
Cytokines
Electron transport chain
Enzyme-linked immunosorbent assay
Epithelial cells
Epithelium
Flow Cytometry
Humans
Interleukin-17 - metabolism
Interleukin-17 - pharmacology
Kinases
Lymphocytes T
Macrophages
Macrophages - cytology
Macrophages - metabolism
Microscopy, Confocal
Mitochondria
Mitochondria - metabolism
Mitophagy
Monocytes
Monocytes - cytology
Monocytes - metabolism
NADH-ubiquinone oxidoreductase
Organophosphorus Compounds - pharmacology
Oxidative stress
Phosphorylation - drug effects
Piperidines - pharmacology
Polarization
Proteins
PTEN-induced putative kinase
Pulmonary fibrosis
Reactive oxygen species
Reactive Oxygen Species - metabolism
Respiratory tract
Respiratory tract diseases
Stimulation
THP-1 Cells
Western blotting
title IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy
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