Abstract
BackgroundAcute exposure to chlorine (Cl2) gas causes epithelial injury and airway dysfunction. γδ T cells are present in the mucosal surface of the airways and may contribute to the injury/repair response of the epithelium.MethodsC57Bl/6J (wild type) and TCR-δ-/- mice exposed to Cl2 (400 ppm) for 5 minutes underwent measurements of airway responses to i.v. methacholine (MCh) at 1, 3, and 5 days after exposure. Bronchoalveolar lavage was performed to determine epithelial and leukocyte counts, and protein content. Tissue repair was assessed by proliferating cell nuclear antigen (PCNA) immunoreactivity and by expression of keratinocyte growth factor (KGF) mRNA by real-time PCR.ResultsWild type mice developed a greater degree of airway hyperresponsiveness to MCh at 1 day post exposure to Cl2 compared with TCR-δ-/- mice. Epithelial cell counts in BAL after Cl2 exposure were greater in TCR-δ-/- mice, but macrophages showed a later peak and granulocyte numbers were lower in TCR-δ-/- than in wild type mice. Both groups had increased levels of total protein content in BAL after Cl2 exposure that resolved after 3 and 5 days, respectively. Epithelial proliferating cell nuclear antigen staining was increased at 1 and 3 days post exposure and was similar in the two groups. KGF mRNA was constitutively expressed in both groups and did not increase significantly after Cl2 but expression was lower in TCR-δ-/- mice.ConclusionThe severity of airway epithelial injury after Cl2 is greater in TCR-δ-/- mice but the inflammatory response and the change in airway responsiveness to methacholine are reduced. The rates of epithelial regeneration are comparable in both groups.
Highlights
Acute exposure to chlorine (Cl2) gas causes epithelial injury and airway dysfunction. γδ T cells are present in the mucosal surface of the airways and may contribute to the injury/repair response of the epithelium
Chlorine exposures were first described in association with chemical warfare, currently most exposures are accidental in industries such as pulp and paper mills
Changes in bronchoalveolar lavage composition after chlorine gas exposure Bronchoalveolar lavage was performed at days 1, 3 and 5 after chlorine exposure
Summary
Acute exposure to chlorine (Cl2) gas causes epithelial injury and airway dysfunction. γδ T cells are present in the mucosal surface of the airways and may contribute to the injury/repair response of the epithelium. Acute exposure to chlorine (Cl2) gas causes epithelial injury and airway dysfunction. Γδ T cells are present in the mucosal surface of the airways and may contribute to the injury/repair response of the epithelium. Effects on epithelial cell function may be associated with chlorine in the swimming pool environment [6]. The effects of acute chlorine gas inhalation in vivo have been investigated in rodent and murine models [7,8]. High concentrations cause early airspace and interstitial edema associated with bronchial epithelial sloughing. Increased lung resistance and/or bronchial hyperresponsiveness to inhaled methacholine have been observed [8]. Changes in lung function relate to the extent of airway epithelial damage and the degree of BAL neutrophilia [7]
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