PMID- 36598904 OWN - NLM STAT- MEDLINE DCOM- 20230106 LR - 20230319 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 18 IP - 1 DP - 2023 TI - Association between serum periostin levels and the severity of arsenic-induced skin lesions. PG - e0279893 LID - 10.1371/journal.pone.0279893 [doi] LID - e0279893 AB - Arsenic is a potent environmental toxicant and human carcinogen. Skin lesions are the most common manifestations of chronic exposure to arsenic. Advanced-stage skin lesions, particularly hyperkeratosis have been recognized as precancerous diseases. However, the underlying mechanism of arsenic-induced skin lesions remains unknown. Periostin, a matricellular protein, is implicated in the pathogenesis of many forms of skin lesions. The objective of this study was to examine whether periostin is associated with arsenic-induced skin lesions. A total of 442 individuals from low- (n = 123) and high-arsenic exposure areas (n = 319) in rural Bangladesh were evaluated for the presence of arsenic-induced skin lesions (Yes/No). Participants with skin lesions were further categorized into two groups: early-stage skin lesions (melanosis and keratosis) and advanced-stage skin lesions (hyperkeratosis). Drinking water, hair, and nail arsenic concentrations were considered as the participants' exposure levels. The higher levels of arsenic and serum periostin were significantly associated with skin lesions. Causal mediation analysis revealed the significant effect of arsenic on skin lesions through the mediator, periostin, suggesting that periostin contributes to the development of skin lesions. When skin lesion was used as a three-category outcome (none, early-stage, and advanced-stage skin lesions), higher serum periostin levels were significantly associated with both early-stage and advanced-stage skin lesions. Median (IQR) periostin levels were progressively increased with the increasing severity of skin lesions. Furthermore, there were general trends in increasing serum type 2 cytokines (IL-4, IL-5, IL-13, and eotaxin) and immunoglobulin E (IgE) levels with the progression of the disease. The median (IQR) of IL-4, IL-5, IL-13, eotaxin, and IgE levels were significantly higher in the early-and advanced-stage skin lesions compared to the group of participants without skin lesions. The results of this study suggest that periostin is implicated in the pathogenesis and progression of arsenic-induced skin lesions through the dysregulation of type 2 immune response. CI - Copyright: (c) 2023 Khatun et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. FAU - Khatun, Moriom AU - Khatun M AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Siddique, Abu Eabrahim AU - Siddique AE AUID- ORCID: 0000-0003-1762-6379 AD - Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York, United States of America. FAU - Wahed, Abdus S AU - Wahed AS AD - Department of Biostatistics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. FAU - Haque, Nazmul AU - Haque N AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Tony, Selim Reza AU - Tony SR AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Islam, Jahidul AU - Islam J AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Alam, Shahnur AU - Alam S AD - Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. FAU - Sarker, Md Khalequzzaman AU - Sarker MK AD - Institute of Biological Sciences, University of Rajshahi, Rajshahi, Bangladesh. FAU - Kabir, Isabela AU - Kabir I AD - Labaid Specialized Hospital, Dhaka, Bangladesh. FAU - Hossain, Shakhawoat AU - Hossain S AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Sumi, Daigo AU - Sumi D AD - Laboratory of Molecular Toxicology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan. FAU - Saud, Zahangir Alam AU - Saud ZA AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. FAU - Barchowsky, Aaron AU - Barchowsky A AD - Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. FAU - Himeno, Seiichiro AU - Himeno S AD - Laboratory of Molecular Toxicology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan. AD - Division of Health Chemistry, School of Pharmacy, Showa University, Tokyo, Japan. FAU - Hossain, Khaled AU - Hossain K AUID- ORCID: 0000-0003-0878-915X AD - Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh. LA - eng SI - figshare/10.6084/m9.figshare.21671057 GR - R01 ES033519/ES/NIEHS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20230104 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - N712M78A8G (Arsenic) RN - 0 (Interleukin-13) RN - 207137-56-2 (Interleukin-4) RN - 0 (Interleukin-5) RN - 37341-29-0 (Immunoglobulin E) SB - IM MH - Humans MH - *Arsenic/toxicity/analysis MH - Interleukin-13 MH - Interleukin-4 MH - Interleukin-5 MH - Environmental Exposure MH - Water Supply MH - *Skin Diseases/chemically induced MH - *Keratosis, Actinic MH - Immunoglobulin E/adverse effects PMC - PMC9812306 COIS- The authors have declared that no competing interests exist. EDAT- 2023/01/05 06:00 MHDA- 2023/01/07 06:00 PMCR- 2023/01/04 CRDT- 2023/01/04 13:33 PHST- 2022/10/01 00:00 [received] PHST- 2022/12/18 00:00 [accepted] PHST- 2023/01/04 13:33 [entrez] PHST- 2023/01/05 06:00 [pubmed] PHST- 2023/01/07 06:00 [medline] PHST- 2023/01/04 00:00 [pmc-release] AID - PONE-D-22-27210 [pii] AID - 10.1371/journal.pone.0279893 [doi] PST - epublish SO - PLoS One. 2023 Jan 4;18(1):e0279893. doi: 10.1371/journal.pone.0279893. eCollection 2023.