Polyhexamethylene guanidine phosphate-induced necrosis may be linked to pulmonary fibrosis
DC Field | Value | Language |
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dc.contributor.author | Kang, Min-Sung | - |
dc.contributor.author | Kim, Sung-Hwan | - |
dc.contributor.author | Yang, Mi-Jin | - |
dc.contributor.author | Kim, Hyeon-Young | - |
dc.contributor.author | Kim, In-Hyeon | - |
dc.contributor.author | Kang, Jeong Won | - |
dc.contributor.author | Choi, Hye-Sook | - |
dc.contributor.author | Jin, Seung-Woo | - |
dc.contributor.author | Park, Eun-Jung | - |
dc.date.accessioned | 2022-08-26T00:40:45Z | - |
dc.date.available | 2022-08-26T00:40:45Z | - |
dc.date.created | 2022-08-25 | - |
dc.date.issued | 2022-06-01 | - |
dc.identifier.issn | 0378-4274 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/143407 | - |
dc.description.abstract | Following the humidifier disinfectant incident in Korea, polyhexamethylene guanidine phosphate (PHMG-P) has been used to establish lung fibrosis model animals. Herein, we investigated time-dependent changes after a single PHMG-P instillation (22 mu g/lung) to identify the underlying pathogenesis and immune response involved in PHMG-P-induced lung fibrosis. Compared to control mice, body weight loss and blood biochemical and hema-tological changes were more remarkable in PHMG-P-instilled mice, an increase of total cell counts, infiltration of macrophages and neutrophils and necrotic cell death were also more notable in the lungs of PHMG-P-instilled mice. Pathological lesions were detected from Day 1 after exposure, deteriorating with time. In addition, secretion of anti-inflammatory mediators was rapidly inhibited from 6 h after exposure, and level of IL-24, a tissue repair-related cytokine, was up-regulated in the lungs of PHMG-P-instilled mice until Day 21 post-exposure. In vitro tests using BEAS-2B cells showed that PHMG-P disturbed structural and functional homeo-stasis of organelles and that intracellular ROS increase was considered as an important cause of PHMG-P-induced cell death. Additionally, co-culture with DNA, a polyanionic compound, clearly inhibited PHMG-P-induced ne-crosis, and increased IL-1 beta and TNF-alpha level and decreased IL-6 and IL-8 levels were observed following exposure to PHMG-P. Meanwhile, IL-8 secretion increased in cells exposed to PHMG-P-induced cell debris. Therefore, we suggest that necrotic cell debris may importantly contribute to the PHMG-P-induced inflammatory response and pathogenesis. In addition, PHMG-P-induced necrosis may be initiated by high affinity between PHMG-P and cell membrane. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER IRELAND LTD | - |
dc.subject | EPITHELIAL-CELLS | - |
dc.subject | LUNG | - |
dc.subject | INFLAMMATION | - |
dc.subject | EXPOSURE | - |
dc.title | Polyhexamethylene guanidine phosphate-induced necrosis may be linked to pulmonary fibrosis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kang, Jeong Won | - |
dc.identifier.doi | 10.1016/j.toxlet.2022.03.009 | - |
dc.identifier.scopusid | 2-s2.0-85129273867 | - |
dc.identifier.wosid | 000797179300001 | - |
dc.identifier.bibliographicCitation | TOXICOLOGY LETTERS, v.362, pp.1 - 16 | - |
dc.relation.isPartOf | TOXICOLOGY LETTERS | - |
dc.citation.title | TOXICOLOGY LETTERS | - |
dc.citation.volume | 362 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 16 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.subject.keywordPlus | EPITHELIAL-CELLS | - |
dc.subject.keywordPlus | LUNG | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | EXPOSURE | - |
dc.subject.keywordAuthor | Polyhexamethylene guanidine | - |
dc.subject.keywordAuthor | Idiopathic pulmonary fibrosis | - |
dc.subject.keywordAuthor | Necrosis | - |
dc.subject.keywordAuthor | Cell death | - |
dc.subject.keywordAuthor | Inflammation | - |
dc.subject.keywordAuthor | Tissue damage | - |
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