Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.

Sulfur mustard (SM) is a cytotoxic, vesicating, chemical warfare agent, first used in 1917; corneas are particularly vulnerable to SM exposure. They may develop inflammation, ulceration, neovascularization (NV), impaired vision, and partial/complete blindness depending upon the concentration of SM,...

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Autores principales:	Dinesh G Goswami, Neha Mishra, Rama Kant, Chapla Agarwal, Claire R Croutch, Robert W Enzenauer, Mark J Petrash, Neera Tewari-Singh, Rajesh Agarwal
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f313f5095bc84e059a03f7fff58a8d07
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spelling	oai:doaj.org-article:f313f5095bc84e059a03f7fff58a8d072021-12-02T20:19:18ZPathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.1932-620310.1371/journal.pone.0258503https://doaj.org/article/f313f5095bc84e059a03f7fff58a8d072021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0258503https://doaj.org/toc/1932-6203Sulfur mustard (SM) is a cytotoxic, vesicating, chemical warfare agent, first used in 1917; corneas are particularly vulnerable to SM exposure. They may develop inflammation, ulceration, neovascularization (NV), impaired vision, and partial/complete blindness depending upon the concentration of SM, exposure duration, and bio-physiological conditions of the eyes. Comprehensive in vivo studies have established ocular structural alterations, opacity, NV, and inflammation upon short durations (<4 min) of SM exposure. In this study, detailed analyses of histopathological alterations in corneal structure, keratocytes, inflammatory cells, blood vessels, and expressions of cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9, vascular endothelial growth factor (VEGF), and cytokines were performed in New Zealand white rabbits, in a time-dependent manner till 28 days, post longer durations (5 and 7 min) of ocular SM exposure to establish quantifiable endpoints of injury and healing. Results indicated that SM exposure led to duration-dependent increases in corneal thickness, opacity, ulceration, epithelial-stromal separation, and epithelial degradation. Significant increases in NV, keratocyte death, blood vessels, and inflammatory markers (COX-2, MMP-9, VEGF, and interleukin-8) were also observed for both exposure durations compared to the controls. Collectively, these findings would benefit in temporal delineation of mechanisms underlying SM-induced corneal toxicity and provide models for testing therapeutic interventions.Dinesh G GoswamiNeha MishraRama KantChapla AgarwalClaire R CroutchRobert W EnzenauerMark J PetrashNeera Tewari-SinghRajesh AgarwalPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 10, p e0258503 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dinesh G Goswami Neha Mishra Rama Kant Chapla Agarwal Claire R Croutch Robert W Enzenauer Mark J Petrash Neera Tewari-Singh Rajesh Agarwal Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
description	Sulfur mustard (SM) is a cytotoxic, vesicating, chemical warfare agent, first used in 1917; corneas are particularly vulnerable to SM exposure. They may develop inflammation, ulceration, neovascularization (NV), impaired vision, and partial/complete blindness depending upon the concentration of SM, exposure duration, and bio-physiological conditions of the eyes. Comprehensive in vivo studies have established ocular structural alterations, opacity, NV, and inflammation upon short durations (<4 min) of SM exposure. In this study, detailed analyses of histopathological alterations in corneal structure, keratocytes, inflammatory cells, blood vessels, and expressions of cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9, vascular endothelial growth factor (VEGF), and cytokines were performed in New Zealand white rabbits, in a time-dependent manner till 28 days, post longer durations (5 and 7 min) of ocular SM exposure to establish quantifiable endpoints of injury and healing. Results indicated that SM exposure led to duration-dependent increases in corneal thickness, opacity, ulceration, epithelial-stromal separation, and epithelial degradation. Significant increases in NV, keratocyte death, blood vessels, and inflammatory markers (COX-2, MMP-9, VEGF, and interleukin-8) were also observed for both exposure durations compared to the controls. Collectively, these findings would benefit in temporal delineation of mechanisms underlying SM-induced corneal toxicity and provide models for testing therapeutic interventions.
format	article
author	Dinesh G Goswami Neha Mishra Rama Kant Chapla Agarwal Claire R Croutch Robert W Enzenauer Mark J Petrash Neera Tewari-Singh Rajesh Agarwal
author_facet	Dinesh G Goswami Neha Mishra Rama Kant Chapla Agarwal Claire R Croutch Robert W Enzenauer Mark J Petrash Neera Tewari-Singh Rajesh Agarwal
author_sort	Dinesh G Goswami
title	Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
title_short	Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
title_full	Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
title_fullStr	Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
title_full_unstemmed	Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
title_sort	pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/f313f5095bc84e059a03f7fff58a8d07
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Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.

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