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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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/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-3bc0143d84f4c7a639ae41cf8f714540f783a34270b7327716cdfe2ea178b7d43</citedby><cites>FETCH-LOGICAL-c412t-3bc0143d84f4c7a639ae41cf8f714540f783a34270b7327716cdfe2ea178b7d43</cites><orcidid>0000-0003-4281-1082 ; 0000-0002-2026-5108 ; 0000-0002-4162-7614 ; 0000-0002-0849-6149</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744791/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8744791/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35008429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsai, Mei-Lan</creatorcontrib><creatorcontrib>Tsai, Yi-Giien</creatorcontrib><creatorcontrib>Lin, Yu-Chih</creatorcontrib><creatorcontrib>Hsu, Ya-Ling</creatorcontrib><creatorcontrib>Chen, Yi-Ting</creatorcontrib><creatorcontrib>Tsai, Ming-Kai</creatorcontrib><creatorcontrib>Liao, Wei-Ting</creatorcontrib><creatorcontrib>Lin, Yi-Ching</creatorcontrib><creatorcontrib>Hung, Chih-Hsing</creatorcontrib><title>IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><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.</description><subject>Acetylcysteine</subject><subject>Acetylcysteine - pharmacology</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Antimycin A - pharmacology</subject><subject>Ascorbic acid</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Asthma</subject><subject>Autophagy</subject><subject>Cell Polarity</subject><subject>Chronic illnesses</subject><subject>Confocal microscopy</subject><subject>Cytokines</subject><subject>Electron transport chain</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-17 - pharmacology</subject><subject>Kinases</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - metabolism</subject><subject>Microscopy, Confocal</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitophagy</subject><subject>Monocytes</subject><subject>Monocytes - cytology</subject><subject>Monocytes - metabolism</subject><subject>NADH-ubiquinone oxidoreductase</subject><subject>Organophosphorus Compounds - pharmacology</subject><subject>Oxidative stress</subject><subject>Phosphorylation - drug effects</subject><subject>Piperidines - pharmacology</subject><subject>Polarization</subject><subject>Proteins</subject><subject>PTEN-induced putative kinase</subject><subject>Pulmonary fibrosis</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Respiratory tract</subject><subject>Respiratory tract diseases</subject><subject>Stimulation</subject><subject>THP-1 Cells</subject><subject>Western blotting</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpd0c1PwjAYBvDGaATRm2ezxIsHp28_oN3FhBA_iBCI6Lnpug5KxorrRoJ_vROQoKe26S9P-vZB6BLDHaUR3Nv5whMKGADoEWpiRkgI0OHHB_sGOvN-DkAoaUenqEHbAIKRqIkm_UFI2kE_TyptkuBtNAmHJrGqrA9DEgyVLtxypqYmGLtMFfZLldblwcqqoDscv4Zd753ecVtu6PocnaQq8-Zit7bQx9Pje-8lHIye-73uINQMkzKksQbMaCJYyjRXHRopw7BORcoxazNIuaCKMsIh5pRwjjs6SQ0xCnMR84TRFnrY5i6reGESbfKyUJlcFnahirV0ysq_N7mdyalbScEZ4xGuA252AYX7rIwv5cJ6bbJM5cZVXpIOFhFEIHhNr__RuauKvB5vowgVXECtbreq_jXvC5PuH4NB_rQlD9uq-dXhAHv8Ww_9BnBpjms</recordid><startdate>20211221</startdate><enddate>20211221</enddate><creator>Tsai, Mei-Lan</creator><creator>Tsai, Yi-Giien</creator><creator>Lin, Yu-Chih</creator><creator>Hsu, Ya-Ling</creator><creator>Chen, Yi-Ting</creator><creator>Tsai, Ming-Kai</creator><creator>Liao, Wei-Ting</creator><creator>Lin, Yi-Ching</creator><creator>Hung, Chih-Hsing</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4281-1082</orcidid><orcidid>https://orcid.org/0000-0002-2026-5108</orcidid><orcidid>https://orcid.org/0000-0002-4162-7614</orcidid><orcidid>https://orcid.org/0000-0002-0849-6149</orcidid></search><sort><creationdate>20211221</creationdate><title>IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-3bc0143d84f4c7a639ae41cf8f714540f783a34270b7327716cdfe2ea178b7d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acetylcysteine</topic><topic>Acetylcysteine - pharmacology</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Antimycin A - pharmacology</topic><topic>Ascorbic acid</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Asthma</topic><topic>Autophagy</topic><topic>Cell Polarity</topic><topic>Chronic illnesses</topic><topic>Confocal microscopy</topic><topic>Cytokines</topic><topic>Electron transport chain</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Interleukin-17 - metabolism</topic><topic>Interleukin-17 - pharmacology</topic><topic>Kinases</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Macrophages - cytology</topic><topic>Macrophages - metabolism</topic><topic>Microscopy, Confocal</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitophagy</topic><topic>Monocytes</topic><topic>Monocytes - cytology</topic><topic>Monocytes - metabolism</topic><topic>NADH-ubiquinone oxidoreductase</topic><topic>Organophosphorus Compounds - pharmacology</topic><topic>Oxidative stress</topic><topic>Phosphorylation - drug effects</topic><topic>Piperidines - pharmacology</topic><topic>Polarization</topic><topic>Proteins</topic><topic>PTEN-induced putative kinase</topic><topic>Pulmonary fibrosis</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Respiratory tract</topic><topic>Respiratory tract diseases</topic><topic>Stimulation</topic><topic>THP-1 Cells</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsai, Mei-Lan</creatorcontrib><creatorcontrib>Tsai, Yi-Giien</creatorcontrib><creatorcontrib>Lin, Yu-Chih</creatorcontrib><creatorcontrib>Hsu, Ya-Ling</creatorcontrib><creatorcontrib>Chen, Yi-Ting</creatorcontrib><creatorcontrib>Tsai, Ming-Kai</creatorcontrib><creatorcontrib>Liao, Wei-Ting</creatorcontrib><creatorcontrib>Lin, Yi-Ching</creatorcontrib><creatorcontrib>Hung, Chih-Hsing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsai, Mei-Lan</au><au>Tsai, Yi-Giien</au><au>Lin, Yu-Chih</au><au>Hsu, Ya-Ling</au><au>Chen, Yi-Ting</au><au>Tsai, Ming-Kai</au><au>Liao, Wei-Ting</au><au>Lin, Yi-Ching</au><au>Hung, Chih-Hsing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-12-21</date><risdate>2021</risdate><volume>23</volume><issue>1</issue><spage>3</spage><pages>3-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>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.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35008429</pmid><doi>10.3390/ijms23010003</doi><orcidid>https://orcid.org/0000-0003-4281-1082</orcidid><orcidid>https://orcid.org/0000-0002-2026-5108</orcidid><orcidid>https://orcid.org/0000-0002-4162-7614</orcidid><orcidid>https://orcid.org/0000-0002-0849-6149</orcidid><oa>free_for_read</oa></addata></record> |
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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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