Heat Stress Elicits Different Responses in Peripheral Blood Mononuclear Cells from Brown Swiss and Holstein Cows

Abstract

This study was undertaken to assess whether peripheral blood mononuclear cells (PBMC) isolated from Brown Swiss (Br) and Holstein (Ho) cows and stimulated with concanavalin A differ in response to chronic exposure to incubation temperatures simulating conditions of hyperthermia. Five multiparous Br and 5 Ho cows were utilized as blood donors. Peripheral blood mononuclear cells were subjected for 65 h to each of 5 treatments (T). Cells were exposed to 39 degrees C continuously (T39) and three 13-h cycles at 40 (T40), 41 (T41), 42 (T42) or 43 degrees C (T43), respectively, which were interspersed with two 13-h cycles at 39 degrees C. Treatment T39 was adopted to mimic normothermia; T40, T41, T42, and T43 mimicked conditions of more severe hyperthermia alternating with normothermia. Measures evaluated at the end of the incubation period were proliferative response (DNA synthesis), intracellular reactive oxygen species (ROS) concentrations, and mRNA abundance of the 72-kDa heat-shock protein (Hsp72). In Br cows, DNA synthesis began to decline when PBMC were repeatedly exposed to 41 degrees C (-22%), whereas DNA synthesis in cells isolated from Ho cows did not begin to decline until 42 degrees C (-40%). Furthermore, under T41 and T42, DNA synthesis from Br cows was lower than in Ho(-24 and -54%, respectively). In both breeds, increased incubation temperatures caused a reduction of intracellular ROS (from -39.6 and -69.7%). Increase in incubation temperatures enhanced Hsp72 mRNA levels only in PBMC isolated from Br cows. The Hsp72 mRNA in Br cows increased significantly under T41 and T43 compared with T39. In both breeds, DNA synthesis was positively and negatively correlated with intracellular ROS and Hsp72 mRNA abundance, respectively (r = 0.85 and r = -0.70, respectively). Results indicated that PBMC from Br cows are less tolerant to chronic heat exposure than those from Ho cows, and that the lower tolerance is associated with higher expression of Hsp72, suggesting that the same level of hyperthermia may be associated with a differential decline of immune function in the 2 breeds.

A comparative study on the expression profile of MCTs and HSPs in Ghungroo and Large White Yorkshire breeds of pigs during different seasons

“…In the present study, we observed that HSP70 mRNA expression was found to be significantly higher (P<0.05) during the summer in both breeds in comparison with the winter season. Our findings are in accordance with previous studies in which heat stress-induced HSP70 expression was observed in the goat PBMCs (Banerjee et al 2014;Dangi et al 2012) and bovine lymphocytes (Lacetera et al 2006;Upadhyay 2007, 2010). During the winter, HSP70 expression was approximately three times higher in Ghungroo compared to LWY.…”

Cellular thermotolerance is associated with heat shock protein 70.1 genetic polymorphisms in Holstein lactating cows

“…One possible approach for reducing the impact of heat stress on cattle productivity is to improve genetic programs that select animals with thermotolerance. Genetic differences in thermotolerance at the physiological and cellular levels are documented by a series of studies on Bos indicus and Bos taurus (Paula-Lopes et al 2003;Hansen 2004;Lacetera et al 2006). Those studies confirm a genetic linkage between species, breed, and individual differences to heat tolerance at the cellular level.…”

Seasonal variations in the composition of Holstein cow’s milk and temperature–humidity index relationship

“…Lacetera et al (2005) observed that summer conditions characterized by the occurrence of extreme events (heat waves) were associated with depressed cellular immunity. Moreover, peripheral blood mononuclear cells, isolated from dairy cows and exposed to incubation temperatures simulating conditions of hyperthermia, exhibited a decrease in DNA synthesis and an increase in heat-shock proteins (Lacetera et al, 2006), indicating a depressed response of cellular-mediated immunity in heat-shock cells.…”