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Polyhexamethylene guanidine phosphate-induced necrosis may be linked to pulmonary fibrosis

Authors
Kang, Min-SungKim, Sung-HwanYang, Mi-JinKim, Hyeon-YoungKim, In-HyeonKang, Jeong WonChoi, Hye-SookJin, Seung-WooPark, Eun-Jung
Issue Date
1-6월-2022
Publisher
ELSEVIER IRELAND LTD
Keywords
Polyhexamethylene guanidine; Idiopathic pulmonary fibrosis; Necrosis; Cell death; Inflammation; Tissue damage
Citation
TOXICOLOGY LETTERS, v.362, pp.1 - 16
Indexed
SCIE
SCOPUS
Journal Title
TOXICOLOGY LETTERS
Volume
362
Start Page
1
End Page
16
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/143407
DOI
10.1016/j.toxlet.2022.03.009
ISSN
0378-4274
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.
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공과대학 (화공생명공학과)
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