Abstract

Simple SummaryThe exposure of animals to excessive heat leads to heat stress, heat stroke, or even death. The first negative effects of heat exposure occur in the gut. The elevated temperature leads to damage in intestinal walls and shifts in the composition of intestinal microbiota. In effect, the gut content (mainly intestinal microbiota and their metabolites) leaks through compromised intestinal walls into milieu of the body. Prebiotics (e.g., GOS—galactooligosaccharides) can be used to mitigate the negative effects of the heat stress in poultry. GOS that are delivered in ovo on day 12 of egg incubation stimulates the development of healthy intestinal microbiota in a chicken embryo. Healthy intestinal microbiota enhances the barrier function of the gut and the immune system. Chickens were originally domesticated in southeast Asia and are therefore genetically adapted to handle high temperatures. However, genetic selection towards performance leads to sensitization to high ambient temperature. In this paper, we studied slow-growing chickens with a reputation for heat resistance. We used in ovo stimulation with the GOS prebiotic that was delivered in ovo to promote healthy gut microbiota. In this manner, we combine genetics and environment to describe a model of heat resistance in poultry.Galactooligosaccharides (GOS) that are delivered in ovo improve intestinal microbiota composition and mitigate the negative effects of heat stress in broiler chickens. Hubbard hybrids are slow-growing chickens with a high resistance to heat. In this paper, we determined the impact of GOS delivered in ovo on slow-growing chickens that are challenged with heat. The experiment was a 2 × 2 × 2 factorial design. On day 12 of incubation, GOS (3.5 mg/egg) was delivered into the egg (n = 300). Controls (C) were mock-injected with physiological saline (n = 300). After hatching, the GOS and C groups were split into thermal groups: thermoneutral (TN) and heat stress (HS). HS (30 °C) lasted for 14 days (days 36–50 post-hatching). The spleen (n = 8) was sampled after acute (8.5 h) and chronic (14 days) HS. The gene expression of immune-related (IL-2, IL-4, IL-6, IL-10, IL-12p40, and IL-17) and stress-related genes (HSP25, HSP90AA1, BAG3, CAT, and SOD) was detected with RT-qPCR. Chronic HS up-regulated the expression of the genes: IL-10, IL-12p40, SOD (p < 0.05), and CAT (p < 0.01). GOS delivered in ovo down-regulated IL-4 (acute p < 0.001; chronic p < 0.01), IL-12p40, CAT and SOD (chronic p < 0.05). The obtained results suggest that slow-growing hybrids are resistant to acute heat and tolerant to chronic heat, which can be supported with in ovo GOS administration.

Highlights

  • Acute and chronic thermal stress significantly hinders the growth performance of poultry [1]

  • In acute Heat stress (HS), among the immune-related genes, only Interleukin 4 (IL-4) responded with differential messenger RNA expression to GOS treatment (p < 0.001), temperature (p < 0.05), and the interactions between those two factors (p < 0.01)

  • In chronic HS, GOS that were delivered in ovo had immunomodulatory effect on: IL-2 (p < 0.05) and IL-4 (p < 0.001)

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Summary

Introduction

Acute and chronic thermal stress significantly hinders the growth performance of poultry [1]. This is due to the fact that the feed intake of chickens that are reared in intensive poultry farms is negatively correlated with environmental temperature [2]. Intensive genetic selection for growth and feed efficiency leads to an increased sensitivity of heavy-weight broilers to environmental conditions, including ambient temperature [4]. Heat stress (HS) could lead to meat quality issues due to increased ante- and post-mortem glycolytic metabolisms coupled with a reduced protein synthesis and turnover, enhanced fat deposition, and the overproduction of reactive oxygen species [10]. Problems related to maintaining optimal temperatures in poultry houses will become more challenging, especially during predicted heat waves, even in moderate climates. Responses to heat vastly depend on the genetic adaptation of the individual [16]

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