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Inhaled sulfur dioxide causes pulmonary and systemic inflammation leading to fibrotic respiratory disease in a rat model of chemical-induced lung injury
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Swedish Defence Research Agency, CBRN Defence and Security, Umeå, Sweden.
2016 (English)In: Toxicology, ISSN 0300-483X, E-ISSN 1879-3185, Vol. 368, 28-36 p.Article in journal (Refereed) Published
Abstract [en]

Inhalation of high concentrations of sulfur dioxide (SO2) affects the lungs and can be immediately dangerous to life. We examined the development of acute and long-term effects after exposure of SO2 in Sprague-Dawley rats, in particular inflammatory responses, airway hyperresponsiveness (AHR) and lung fibrosis. Animals were subjected to a single exposure of 2200 ppm SO2 during 10 min and treated with a single dose of the anti-inflammatory corticosteroid dexamethasone 1 h following exposure. Exposed rats showed labored breathing, decreased body-weight and an acute inflammation with neutrophil and macrophage airway infiltrates 5 h post exposure. The acute effects were characterized by bronchial damage restricted to the larger bronchi with widespread injured mucosal epithelial lining. Rats displayed hyperreactive airways 24 h after exposure as indicated by increased methacholine-induced respiratory resistance. The inflammatory infiltrates remained in lung tissue for at least 14 days but at the late time-point the dominating granulocyte types had changed from neutrophils to eosinophils. Analysis of immunoregulatory and pro-inflammatory cytokines in serum and airways implicated mixed macrophage phenotypes (M-1/M-2) and T helper cell activation of both T(H)1 and T(H)2 subtypes. Increased expression of the pro-fibrotic cytokine TGF beta 1 was detected in airways 24 h post exposure and remained increased at the late time-points (14 and 28 days). The histopathology analysis confirmed a significant collagen deposition 14 days post exposure. Treatment with dexamethasone significantly counteracted the acute inflammatory response but was insufficient for complete protection against SO2-induced adverse effects, i.e. treatment only provided partial protection against AHR and the long-term fibrosis.

Place, publisher, year, edition, pages
2016. Vol. 368, 28-36 p.
National Category
Clinical Medicine
Identifiers
URN: urn:nbn:se:umu:diva-128481DOI: 10.1016/j.tox.2016.08.018ISI: 000387199300004PubMedID: 27565714OAI: oai:DiVA.org:umu-128481DiVA: diva2:1056583
Available from: 2016-12-15 Created: 2016-12-05 Last updated: 2016-12-15Bibliographically approved

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CiteExportLink to record
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Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
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  • de-DE
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