Heat stress impairs performance parameters, induces intestinal injury, and decreases macrophage activity in broiler chickens

TLDR

Environmental stress research has expanded due to economic and welfare concerns, and heat stress in broiler chickens is known to cause physiological, hormonal, and immune deficits that increase disease susceptibility. The study aimed to evaluate how two heat stress regimes (31 ± 1 °C and 36 ± 1 °C) affect corticosterone, growth performance, intestinal histology, and macrophage activity in broilers from day 35 to 42. Broilers were exposed to 31 ± 1 °C or 36 ± 1 °C for 10 h/day between days 35 and 42, while corticosterone levels, growth metrics, gut tissue, and macrophage responses were measured and analyzed under a neuroimmune framework. Heat stress increased corticosterone, decreased body weight gain and feed intake, and at 36 °C worsened feed conversion and raised mortality; both temperatures reduced bursa, thymus, and spleen weights and impaired macrophage activity, while 36 °C induced mild enteritis, all linked to HPA axis activation and highlighting neuroimmune pathways that could enhance broiler welfare and productivity.

Abstract

Studies on environmental consequences of stress on animal production have grown substantially in the last few years for economic and animal welfare reasons. Physiological, hormonal, and immunological deficits as well as increases in animals' susceptibility to diseases have been reported after different stressors in broiler chickens. The aim of the current experiment is to describe the effects of 2 different heat stressors (31 +/- 1 and 36 +/- 1 degrees C/10 h per d) applied to broiler chickens from d 35 to 42 of life on the corticosterone serum levels, performance parameters, intestinal histology, and peritoneal macrophage activity, correlating and discussing the obtained data under a neuroimmune perspective. In our study, we demonstrated that heat stress (31 +/- 1 and 36 +/- 1 degrees C) increased the corticosterone serum levels and decreased BW gain and food intake. Only chickens submitted to 36 +/- 1 degrees C, however, presented a decrease in feed conversion and increased mortality. We also showed a decrease of bursa of Fabricius (31 +/- 1 and 36 +/- 1 degrees C), thymus (36 +/- 1 degrees C), and spleen (36 +/- 1 degrees C) relative weights and of macrophage basal (31 +/- 1 and 36 +/- 1 degrees C) and Staphylococcus aureus-induced oxidative burst (31 +/- 1 degrees C). Finally, mild multifocal acute enteritis characterized by an increased presence of lymphocytes and plasmocytes within the jejunum's lamina propria was also observed. The stress-induced hypothalamic-pituitary-adrenal axis activation was taken as responsible for the negative effects observed on the chickens' performance and immune function and also the changes of the intestinal mucosa. The present obtained data corroborate with others in the field of neuroimmunomodulation and open new avenues for the improvement of broiler chicken welfare and production performance.