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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 Cl2compared with TCR-δ-/-mice. Epithelial cell counts in BAL after Cl2exposure 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 Cl2exposure 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 Cl2but expression was lower in TCR-δ-/-mice.ConclusionThe severity of airway epithelial injury after Cl2is 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.