PS2-3. β-defensins Gene Expression in Nasal Mucosal Secretions of Calves with Bovine Respiratory Disease by Elevated Body Temperature.

Abstract Bovine respiratory disease (BRD) is the most economically significant disease in the U.S. cattle industry, resulting in greater financial losses than any other illness. Although vaccination and antibiotic treatments are commonly used, they are not always effective due to the variety of BRD-causing pathogens, and excessive antibiotic use may contribute to antibiotic resistance. Therefore, alternative approaches that focus on microbial and immune system mechanisms may provide more effective strategies for reducing BRD. Defensins are antimicrobial proteins produced during the innate immune response, and β-defensins are secreted by mucosal epithelial cells in tissues. The objective of this study was to determine β-defensin expression in nasal mucosal secretions of calves affected by BRD. Post-weaned crossbred beef calves (n = 9; average BW 278.1 ± 36 kg) were evaluated for mucosal β-defensin expression. Nasal swabs and rectal temperatures were collected on d 0, 1, 2, and 3 at 0800 h. Rectal temperature was used to assign BRD status each day where ‘sick’ calves had a rectal temperate ≥ 39.4 °C while ‘healthy’ had a rectal temperature < 39.4 °C. Relative expression of β-defensins DEFB401, DEFB402, and DEFB403 from nasal swabs was determined using qPCR and calculated using the 2-ΔΔCt method. Data were analyzed using the GLIMMIX procedure of SAS. Significance was declared at P ≤ 0.05. β-defensin expression in nasal mucosal secretions did not differ between healthy and sick calves. More specifically, there was no effect of BRD status on expression of DEFB401 (P = 0.63), DEFB402 (P = 0.34), or DEFB403 (P = 0.92). These results suggest that the β-defensins measured in the current study do not differ between calves diagnosed with BRD based on elevated rectal temperature. Therefore, future research is warranted to understand the mechanisms of DEFB 401, 402, and 403 defensins as well as identifying additional β-defensins that might interact with innate host immunity against BRD.