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Acute respiratory changes and pulmonary inflammation involving a pathway of TGF-beta 1 induction in a rat model of chlorine-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.
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2016 (English)In: Toxicology and Applied Pharmacology, ISSN 0041-008X, E-ISSN 1096-0333, Vol. 309, 44-54 p.Article in journal (Refereed) Published
Abstract [en]

We investigated acute and delayed respiratory changes after inhalation exposure to chlorine (Cl-2) with the aim to understand the pathogenesis of the long-term sequelae of Cl-2-induced lung-injury. In a rat model of nose-only exposure we analyzed changes in airway hyperresponsiveness (AHR), inflammatory responses in airways, expression of pro-inflammatory markers and development of lung fibrosis during a time course from 5 h up to 90 days after a single inhalation of Cl-2. A single dose of dexamethasone (10 mg/Kg) was administered 1 h following Cl-2-exposure. A 15-min inhalation of 200 ppm Cl-2 was non-lethal in Sprague-Dawley rats. At 24 h post exposure, Cl-2-exposed rats displayed elevated numbers of leukocytes with an increase of neutrophils and eosinophils in bronchoalveolar lavage (BAL) and edema was shown both in lung tissue and the heart At 24 h, the inflammasome-associated cytokines IL-1 beta and IL-18 were detected in BAL Concomitant with the acute inflammation a significant AHR was detected. At the later time-points, a delayed inflammatory response was observed together with signs of lung fibrosis as indicated by increased pulmonary macrophages, elevated TGF-beta expression in BAL and collagen deposition around airways. Dexamethasone reduced the numbers of neutrophils in BAL at 24 h but did not influence the AHR. Inhalation of Cl-2 in rats leads to acute respiratory and cardiac changes as well as pulmonary inflammation involving induction of TGF-beta 1. The acute inflammatory response was followed by sustained macrophage response and lack of tissue repair. It was also found that pathways apart from the acute inflammatory response contribute to the Cl(2-)induced respiratory dysfunction. 

Place, publisher, year, edition, pages
2016. Vol. 309, 44-54 p.
Keyword [en]
Chlorine, Chemical-induced lung injury, Airway hyperresponsiveness, Respiratory mechanics, flammation
National Category
Respiratory Medicine and Allergy
Identifiers
URN: urn:nbn:se:umu:diva-127946DOI: 10.1016/j.taap.2016.08.027ISI: 000384510800006PubMedID: 27586366OAI: oai:DiVA.org:umu-127946DiVA: diva2:1059275
Available from: 2016-12-22 Created: 2016-11-21 Last updated: 2016-12-22Bibliographically approved

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CiteExportLink to record
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Citation style
  • apa
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