Inhaled Kathon may induce eosinophilia‐mediated disease in the lung
In 2011, a link between humidifier disinfectants and patients with idiopathic pulmonary fibrosis was identified in Korea, and Kathon was suggested as one of the causative agents. In this study, Kathon induced apoptotic cell death along with membrane damage at 24 h post‐exposure. Additionally, on day...
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| Veröffentlicht in: | Environmental toxicology 2020-01, Vol.35 (1), p.27-36 |
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| creator | Park, Eun‐Jung Han, Ji‐Seok Seong, Eunsol Park, Eun‐Jun Lee, Byoung‐Seok Lee, Sang Jin Lee, Kyuhong |
| description | In 2011, a link between humidifier disinfectants and patients with idiopathic pulmonary fibrosis was identified in Korea, and Kathon was suggested as one of the causative agents. In this study, Kathon induced apoptotic cell death along with membrane damage at 24 h post‐exposure. Additionally, on day 14 after a single instillation with Kathon, the total number of pulmonary cells and the levels of TNF‐α, IL‐5, IL‐13, MIP‐1α, and MCP‐1α clearly increased in the lung of mice. The proportion of natural killer cells and eosinophils were significantly elevated in the spleen and the bloodstream, respectively, and the level of immunoglobulin (Ig) A, but not IgG, IgM, and IgE, dose‐dependently increased. Therefore, we suggest that inhaled Kathon may induce eosinophilia‐mediated disease in the lung by disrupting homeostasis of pulmonary surfactants. Considering that eosinophilia is closely related to cancer and fibrosis, further studies are needed to understand the relationship between them. |
| doi_str_mv | 10.1002/tox.22839 |
| format | Article |
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In this study, Kathon induced apoptotic cell death along with membrane damage at 24 h post‐exposure. Additionally, on day 14 after a single instillation with Kathon, the total number of pulmonary cells and the levels of TNF‐α, IL‐5, IL‐13, MIP‐1α, and MCP‐1α clearly increased in the lung of mice. The proportion of natural killer cells and eosinophils were significantly elevated in the spleen and the bloodstream, respectively, and the level of immunoglobulin (Ig) A, but not IgG, IgM, and IgE, dose‐dependently increased. Therefore, we suggest that inhaled Kathon may induce eosinophilia‐mediated disease in the lung by disrupting homeostasis of pulmonary surfactants. Considering that eosinophilia is closely related to cancer and fibrosis, further studies are needed to understand the relationship between them.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.22839</identifier><identifier>PMID: 31498972</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Blood diseases ; Cancer ; Cell death ; Cell Line ; chloromethylisothiazolone ; Cytokines - immunology ; Disinfectants ; Disinfectants - toxicity ; Disruption ; Eosinophilia ; Eosinophilia - blood ; Eosinophilia - chemically induced ; Eosinophilia - immunology ; Eosinophils ; Eosinophils - cytology ; Fibrosis ; Homeostasis ; Humans ; immunoglobulin A ; Immunoglobulin A - blood ; Immunoglobulin E ; Immunoglobulin G ; Immunoglobulin M ; Inhalation Exposure - adverse effects ; Leukocytes (eosinophilic) ; Lung - drug effects ; Lung - immunology ; Lung - metabolism ; Lung - pathology ; Lung diseases ; Lungs ; Male ; matrix metalloproteinase ; methylisothiazolinone ; Mice ; Mice, Inbred ICR ; Natural killer cells ; Pollutants ; Pulmonary Surfactants - metabolism ; Spleen ; Surfactants ; Thiazoles - toxicity ; Tumor necrosis factor</subject><ispartof>Environmental toxicology, 2020-01, Vol.35 (1), p.27-36</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4119-72af048f14be7d634b44f67b622e593ae8c45ab562edda237351b335d7e2cc833</citedby><cites>FETCH-LOGICAL-c4119-72af048f14be7d634b44f67b622e593ae8c45ab562edda237351b335d7e2cc833</cites><orcidid>0000-0002-3723-5351</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.22839$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.22839$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31498972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Eun‐Jung</creatorcontrib><creatorcontrib>Han, Ji‐Seok</creatorcontrib><creatorcontrib>Seong, Eunsol</creatorcontrib><creatorcontrib>Park, Eun‐Jun</creatorcontrib><creatorcontrib>Lee, Byoung‐Seok</creatorcontrib><creatorcontrib>Lee, Sang Jin</creatorcontrib><creatorcontrib>Lee, Kyuhong</creatorcontrib><title>Inhaled Kathon may induce eosinophilia‐mediated disease in the lung</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>In 2011, a link between humidifier disinfectants and patients with idiopathic pulmonary fibrosis was identified in Korea, and Kathon was suggested as one of the causative agents. In this study, Kathon induced apoptotic cell death along with membrane damage at 24 h post‐exposure. Additionally, on day 14 after a single instillation with Kathon, the total number of pulmonary cells and the levels of TNF‐α, IL‐5, IL‐13, MIP‐1α, and MCP‐1α clearly increased in the lung of mice. The proportion of natural killer cells and eosinophils were significantly elevated in the spleen and the bloodstream, respectively, and the level of immunoglobulin (Ig) A, but not IgG, IgM, and IgE, dose‐dependently increased. Therefore, we suggest that inhaled Kathon may induce eosinophilia‐mediated disease in the lung by disrupting homeostasis of pulmonary surfactants. Considering that eosinophilia is closely related to cancer and fibrosis, further studies are needed to understand the relationship between them.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Blood diseases</subject><subject>Cancer</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>chloromethylisothiazolone</subject><subject>Cytokines - immunology</subject><subject>Disinfectants</subject><subject>Disinfectants - toxicity</subject><subject>Disruption</subject><subject>Eosinophilia</subject><subject>Eosinophilia - blood</subject><subject>Eosinophilia - chemically induced</subject><subject>Eosinophilia - immunology</subject><subject>Eosinophils</subject><subject>Eosinophils - cytology</subject><subject>Fibrosis</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>immunoglobulin A</subject><subject>Immunoglobulin A - blood</subject><subject>Immunoglobulin E</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin M</subject><subject>Inhalation Exposure - adverse effects</subject><subject>Leukocytes (eosinophilic)</subject><subject>Lung - drug effects</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Male</subject><subject>matrix metalloproteinase</subject><subject>methylisothiazolinone</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Natural killer cells</subject><subject>Pollutants</subject><subject>Pulmonary Surfactants - metabolism</subject><subject>Spleen</subject><subject>Surfactants</subject><subject>Thiazoles - toxicity</subject><subject>Tumor necrosis factor</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kLtOwzAUQC0EoqUw8AMoEhNDWj8TZ0RVgYpKXYrEZjnxDXGVJiVOBN34BL6RL8E0hY3Jdzg69_ogdEnwmGBMJ239PqZUsuQIDYmgNIxpLI_3Mw45lmSAzpxbY4yTSESnaMAIT2QS0yGazatCl2CCR90WdRVs9C6wlekyCKB2tqq3hS2t_vr43ICxuvWksQ60A48FbQFB2VUv5-gk16WDi8M7Qk93s9X0IVws7-fT20WYcUISf5bOMZc54SnEJmI85TyP4jSiFETCNMiMC52KiIIxmrKYCZIyJkwMNMskYyN03Xu3Tf3agWvVuu6ayq9UlFHCcSRF7Kmbnsqa2rkGcrVt7EY3O0Ww-gmmfDC1D-bZq4OxS_0P_8jfQh6Y9MCbLWH3v0mtls-98hvVEnUQ</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Park, Eun‐Jung</creator><creator>Han, Ji‐Seok</creator><creator>Seong, Eunsol</creator><creator>Park, Eun‐Jun</creator><creator>Lee, Byoung‐Seok</creator><creator>Lee, Sang Jin</creator><creator>Lee, Kyuhong</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</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>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><orcidid>https://orcid.org/0000-0002-3723-5351</orcidid></search><sort><creationdate>202001</creationdate><title>Inhaled Kathon may induce eosinophilia‐mediated disease in the lung</title><author>Park, Eun‐Jung ; Han, Ji‐Seok ; Seong, Eunsol ; Park, Eun‐Jun ; Lee, Byoung‐Seok ; Lee, Sang Jin ; Lee, Kyuhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4119-72af048f14be7d634b44f67b622e593ae8c45ab562edda237351b335d7e2cc833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Blood diseases</topic><topic>Cancer</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>chloromethylisothiazolone</topic><topic>Cytokines - immunology</topic><topic>Disinfectants</topic><topic>Disinfectants - toxicity</topic><topic>Disruption</topic><topic>Eosinophilia</topic><topic>Eosinophilia - blood</topic><topic>Eosinophilia - chemically induced</topic><topic>Eosinophilia - immunology</topic><topic>Eosinophils</topic><topic>Eosinophils - cytology</topic><topic>Fibrosis</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>immunoglobulin A</topic><topic>Immunoglobulin A - blood</topic><topic>Immunoglobulin E</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin M</topic><topic>Inhalation Exposure - adverse effects</topic><topic>Leukocytes (eosinophilic)</topic><topic>Lung - drug effects</topic><topic>Lung - immunology</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Male</topic><topic>matrix metalloproteinase</topic><topic>methylisothiazolinone</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Natural killer cells</topic><topic>Pollutants</topic><topic>Pulmonary Surfactants - metabolism</topic><topic>Spleen</topic><topic>Surfactants</topic><topic>Thiazoles - toxicity</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Eun‐Jung</creatorcontrib><creatorcontrib>Han, Ji‐Seok</creatorcontrib><creatorcontrib>Seong, Eunsol</creatorcontrib><creatorcontrib>Park, Eun‐Jun</creatorcontrib><creatorcontrib>Lee, Byoung‐Seok</creatorcontrib><creatorcontrib>Lee, Sang Jin</creatorcontrib><creatorcontrib>Lee, Kyuhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Eun‐Jung</au><au>Han, Ji‐Seok</au><au>Seong, Eunsol</au><au>Park, Eun‐Jun</au><au>Lee, Byoung‐Seok</au><au>Lee, Sang Jin</au><au>Lee, Kyuhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhaled Kathon may induce eosinophilia‐mediated disease in the lung</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2020-01</date><risdate>2020</risdate><volume>35</volume><issue>1</issue><spage>27</spage><epage>36</epage><pages>27-36</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract>In 2011, a link between humidifier disinfectants and patients with idiopathic pulmonary fibrosis was identified in Korea, and Kathon was suggested as one of the causative agents. In this study, Kathon induced apoptotic cell death along with membrane damage at 24 h post‐exposure. Additionally, on day 14 after a single instillation with Kathon, the total number of pulmonary cells and the levels of TNF‐α, IL‐5, IL‐13, MIP‐1α, and MCP‐1α clearly increased in the lung of mice. The proportion of natural killer cells and eosinophils were significantly elevated in the spleen and the bloodstream, respectively, and the level of immunoglobulin (Ig) A, but not IgG, IgM, and IgE, dose‐dependently increased. Therefore, we suggest that inhaled Kathon may induce eosinophilia‐mediated disease in the lung by disrupting homeostasis of pulmonary surfactants. Considering that eosinophilia is closely related to cancer and fibrosis, further studies are needed to understand the relationship between them.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>31498972</pmid><doi>10.1002/tox.22839</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-3723-5351</orcidid></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Blood diseases Cancer Cell death Cell Line chloromethylisothiazolone Cytokines - immunology Disinfectants Disinfectants - toxicity Disruption Eosinophilia Eosinophilia - blood Eosinophilia - chemically induced Eosinophilia - immunology Eosinophils Eosinophils - cytology Fibrosis Homeostasis Humans immunoglobulin A Immunoglobulin A - blood Immunoglobulin E Immunoglobulin G Immunoglobulin M Inhalation Exposure - adverse effects Leukocytes (eosinophilic) Lung - drug effects Lung - immunology Lung - metabolism Lung - pathology Lung diseases Lungs Male matrix metalloproteinase methylisothiazolinone Mice Mice, Inbred ICR Natural killer cells Pollutants Pulmonary Surfactants - metabolism Spleen Surfactants Thiazoles - toxicity Tumor necrosis factor |
| title | Inhaled Kathon may induce eosinophilia‐mediated disease in the lung |
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