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LeakyCow – Heat stress-induced local and systemic immune responses in dairy cows with `leaky gut syndrome`

Applicant Dr. Franziska Koch
Subject Area Animal Breeding, Animal Nutrition, Animal Husbandry
Term from 2020 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 441013809
 
Final Report Year 2024

Final Report Abstract

Climate change is expected to increase the frequency of extreme weather events, such as heat waves, in the coming years. Heat-stressed dairy cows reduce feed intake, milk yield, reproductive performance and are at increased risk of diseases. In order to increase heat loss, the blood circulation is directed away from the visceral area towards the skin. The local blood flow in the splanchnic area is reduced, leading to local hypoxia episodes in the gastrointestinal tract, increasing gut permeability. However, little is known about the onset of a local and/or systemic immune response activated by penetrated pathogens and bacteria from the gastrointestinal tract, and whether the increase in ambient temperature might also lead to microbial dysbiosis linking endotoxemia, `leaky gut` and immune response. The aim of this study was to elucidate the negative effects of high ambient temperatures on the humoral immune response in mesenteric lymph nodes and peripheral blood mononuclear cells (PBMCs) and its interaction with the intestinal gut microbiota in lactating Holstein cows. Thirty dairy cows were assigned to either a control (CON; 16°C, temperaturehumidity-index (THI) 60, ad libitum), heat-stressed (HS; 28°C, THI 76, ad libitum) or pair-feeding (PF; 16°C, THI 60, restricted feeding to HS cows) group for seven days of treatment. The PF group mirrored the reduced feed intake behaviour of the HS group. The local immune response in the mesenteric lymph nodes (MLN) were characterized by the activation of the Toll-like receptor 2 signaling pathway, which induce proinflammatory cytokine production, e.g. tumor necrosis factor α (TNFα) and interferon γ (IFNγ). However, chemokines regulating the leucocyte trafficking between the MLN and the gut seem not to be involved in the adaptive immune response to heat stress. In the systemic blood circulation, proinflammatory cytokines and the acute phase protein haptoglobin were induced by circulating endotoxin. Furthermore, RNA sequencing of PBMCs revealed that heat stress activates vasoconstriction, platelet activation and the coagulation cascade with concomitant leucocyte trafficking during heat stress, potentially caused by microvascular injuries and fluid shear stress due to altered blood flow. Moreover, specific immune pathways related to the T cell receptor signaling pathway, antigen processing and presentation, and intestinal immune network for IgA production, as well as metabolic pathways related to lysine degradation and lipid metabolism, were down-regulated, implying immunosuppression of lymphocytes and metabolic adaptation to lower nutrient availability during HS. Moreover, the reduction in feed intake during HS had significant effects on microbial diversity and the abundance of certain taxa, e.g. unclassified Clostridia, Succinivibrionaceae UCG-001, Colidextribacter, Lachnospiraceae UCG-008, which could provide a potential source of pathogens and messenger molecules facilitating the activation of the immune response in the gastrointestinal tract, underpinning the importance of maintaining intestinal homeostasis.

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