Mild heat stress-induced adaptive immune response in blood mononuclear cells and leukocytes from mesenteric lymph nodes of primiparous lactating Holstein cows

Heat stress negatively affects the metabolism and physiology of the bovine gut. However, it is not known whether heat stress induces an inflammatory response in mesenteric lymph nodes (MLN), the primary origin of gut immune cells, and thus contributes to inflam-matory processes in the circulation. Therefore, our objective was to elucidate the effects of chronic heat stress on the systemic activation of acute-phase re-sponse in blood, proinflammatory cytokine production in peripheral blood mononuclear cells (PBMC), and the activation of the toll-like receptor signaling (TLR) 2/4 pathway in MLN leucocytes and their chemokines and chemokine receptor profiles in Holstein cows. Primipa-rous Holstein cows (n = 30; 169 +/- 9 d in milk) were exposed to a temperature-humidity index (THI) of 60 [16 degrees C, 63% relative humidity (RH)] for 6 d. Thereafter, cows were evenly assigned to 3 groups: heat-stressed (HS; 28 degrees C, 50% RH, THI = 76), control (CON; 16 degrees C, 69% RH, THI = 60), or pair-feeding (PF; 16 degrees C, 69% RH, THI = 60) for 7 d. On d 6, PBMC were isolated and on d 7 MLN. Plasma haptoglobin, TNF alpha, and IFN gamma concentrations increased more in HS than CON cows. Concomitantly, TNFA mRNA abundance was higher in PBMC and MLN leucocytes of HS than PF cows, whereas IFNG mRNA abundance tended to be higher in MLN leucocytes of HS than PF cows, but not for chemokines (CCL20, CCL25) or chemokine recep-tors (ITGB7, CCR6, CCR7, CCR9). Furthermore, the TLR2 protein expression tended to be more abundant in MLN leucocytes of HS than PF cows. These results suggest that heat stress induced an adaptive immune response in blood, PBMC, and MLN leukocytes involv-ing the acute-phase protein haptoglobin, proinflam- matory cytokine production, and TLR2 signaling in MLN leucocytes. However, chemokines regulating the leucocyte trafficking between MLN and gut seem not to be involved in the adaptive immune response to heat stress.