Bovine respiratory syncytial virus-specific IgE is associated with interleukin-2 and -4, and interferon-γ expression in pulmonary lymph of experimentally infected calves
- 1 March 2000
- journal article
- Published by American Veterinary Medical Association (AVMA) in American Journal of Veterinary Research
- Vol. 61 (3) , 291-298
- https://doi.org/10.2460/ajvr.2000.61.291
Abstract
Objective—To study the local immune response of calves to bovine respiratory syncytial virus (BRSV) infection with emphasis on IgE production and cytokine gene expression in pulmonary lymph.Animals—Twelve 6- to 8-week-old Holstein bull calves. Six similar control calves were mock infected to obtain control data.Procedure—Lymphatic cannulation surgery was performed on 12 calves to create a long-term thoracic lymph fistula draining to the exterior. Cannulated calves were exposed to virulent BRSV by aerosol. Lymph fluid collected daily was assayed for BRSV and isotype-specific IgE antibody, total IgG, IgA, IgM, and protein concentrations. Interleukin-4 (IL-4), interleukin- 2 (IL-2), and interferon-γ were semi-quantitated by reverse transcription-polymerase chain reaction (RT-PCR). Cell counts and fluorescence-activated cell scanner (FACSCAN) analysis of T-cell subsets were performed on lymph cells.Results—Calves had clinical signs of respiratory tract disease during days 5 to 10 after infection and shed virus. Bovine respiratory syncytial virus-specific IgE in infected calves was significantly increased over baseline on day 9 after infection. Mean virus-specific IgE concentrations strongly correlated with increases in severity of clinical disease (r = 0.903). Expression of IL-2, IL-4, and interferon-γ was variably present in infected and control calves, with IL-4 expression most consistent during early infection.Conclusions and Clinical Relevance—Infection with BRSV was associated with production of BRSV-specific IgE, and IL-4 message was commonly found in lymph cells of infected calves. This finding supports the concept that BRSV-induced pathophysiology involves a T helper cell type-2 response. Effective therapeutic and prophylactic strategies could, therefore, be developed using immunomodulation to shift the immune response more toward a T helper cell type-1 response. (Am J Vet Res2000;61:291–298)Keywords
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