Abstract

Simple SummaryHeat stress affects animal husbandry by impeding the health and production of livestock and leads to commercial losses during the hot summer season. The broiler chicken is one variety of poultry that is bred and reared for commercial meat production, but exposing this breed to high environmental temperatures causes immunosuppression. To improve heat stress tolerance in broilers, thermal manipulation (TM), a process which involves timed changes in incubation temperature during embryonic development, has been suggested as a way to enhance thermotolerance acquisition and immune response. Cytokines are small extracellular signaling peptides with critical roles in immunity by enabling cell communication during immunological development and an immune response. The objective of the current study was to investigate the effects of TM during broiler chicken embryonic development on splenic mRNA levels of the Interferon-α (IFN-α), Interferon- β (IFN-β), Interferon- γ (IFN-γ), Interleukin-4 (IL-4), Interleukin-8 (IL-8), Interleukin-15 (IL-15), Interleukin-16 (IL-16), Interleukin-17 (IL-17), and Interleukin-18 (IL-18) genes during acute heat stress (AHS). Our findings suggest that TM has a long-term effect on cytokine expression dynamics during AHS. Consequently, TM may improve heat tolerance acquisition by increasing the expression of signaling proteins important to tissue stability as well as to repair mechanisms that are employed during and/or after heat stress recovery.Heat stress significantly impacts the immunity and cytokine expression of chickens. However, the effects of embryonic thermal manipulation (TM) on cytokine expression in broiler chickens (broilers) is unclear. The objective of the current study was to evaluate the effects of TM on the splenic mRNA expression dynamics of certain cytokines—namely, IFN-α, IFN-β, IFN-γ, IL-4, IL-8, IL-15, IL-16, IL-17, and IL-18—in broilers during subsequent exposure to acute heat stress (AHS). TM was performed by elevating the incubation temperature to 39 °C at 65% relative humidity (RH) for 18 h daily during embryonic days (ED) 10–18. On post-hatch day 28, AHS was carried out for 7 h at 40 °C. At 0 h and after 1, 3, 5, and 7 h of AHS, splenic tissues were collected from all study groups to evaluate mRNA expression by relative-quantitative real-time (RT)-PCR. Plasma was collected to measure IL-4, IL-8, and IFN-γ levels. At 0 h, TM significantly reduced the basal mRNA level of IFN-β and the plasma level of IFN-γ and IL-8. Moreover, AHS significantly decreased IFN-β in control chicks, decreased IL-4 in both TM and control chicks, and increased IFN-γ and IL-16 in TM chicks. IFN-α, IL-8, IL-15, IL-17, and IL-18 expression all significantly increased during AHS in both TM and control chicks, but expression dynamics were improved in TM chicks for all cytokines (except IL-17). AHS resulted in increased plasma IFN-γ levels in TM chicks only, and increased IL-8 levels at 3 and 5 h of AHS in TM chicks, but at 7 h in control chicks. Lastly, 3 h of AHS increased IL-4 plasma levels in control chicks. The results of this study may indicate that TM has a long-term effect on cytokine expression dynamics of broilers, especially during AHS. Therefore, TM may improve heat tolerance acquisition by increasing the expression of signaling proteins important to tissue stability and to repair mechanisms that are employed during and/or after heat stress recovery.

Highlights

  • Heat stress affects animal husbandry by impeding the health and production of livestock, leading to commercial losses during hot summer seasons [1]

  • It was found that Thermal Manipulation (TM) during broiler embryogenesis led to a significantly lower hatchability rate

  • The aim of the current study was to examine the impact of TM (39 ◦ C and 65% relative humidity (RH) for 18 h daily during embryonic days (ED) 10 to 18) and subsequent acute heat stress (AHS) on the splenic mRNA expression of the IFN-α, IFN-β, IFN-γ, IL-4, IL-8, IL-15, IL-16, IL-17, and IL-18 cytokines, as well as on the plasma levels of IFN-γ, IL-4, and IL-8, in broiler chickens

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Summary

Introduction

Heat stress affects animal husbandry by impeding the health and production of livestock, leading to commercial losses during hot summer seasons [1]. Exposing broiler chickens (broilers) to high environmental temperatures results in immunosuppression through the dual activation of the sympathetic nervous system alongside the hypothalamic–pituitary–adrenal axis, leading to high catecholamine and corticosterone serum levels [2,3,4]. Heat stress was found to modulate the gene expression of a range of different cytokines in broiler chickens [5,6]. Cytokines are small extracellular signaling peptides which have been shown to play a critical role in immunity [7,8]. In addition to the above, cytokines play an important role in healing injured tissue, including insults arising as a result of heat stroke [11,12]. Heat stress has been found to modulate the splenic and intestinal gene expression of several different types of cytokines in chickens [5,13,14]

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