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Vladimir Zmrhal
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Zmrhal, V.; Svoradova, A.; Venusova, E.; Slama, P. Influence of Heat Stress on Chicken Immune System. Encyclopedia. Available online: https://encyclopedia.pub/entry/48065 (accessed on 08 July 2024).
Zmrhal V, Svoradova A, Venusova E, Slama P. Influence of Heat Stress on Chicken Immune System. Encyclopedia. Available at: https://encyclopedia.pub/entry/48065. Accessed July 08, 2024.
Zmrhal, Vladimir, Andrea Svoradova, Eva Venusova, Petr Slama. "Influence of Heat Stress on Chicken Immune System" Encyclopedia, https://encyclopedia.pub/entry/48065 (accessed July 08, 2024).
Zmrhal, V., Svoradova, A., Venusova, E., & Slama, P. (2023, August 15). Influence of Heat Stress on Chicken Immune System. In Encyclopedia. https://encyclopedia.pub/entry/48065
Zmrhal, Vladimir, et al. "Influence of Heat Stress on Chicken Immune System." Encyclopedia. Web. 15 August, 2023.
Influence of Heat Stress on Chicken Immune System
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This entry is adapted from the peer-reviewed paper 10.3390/ani13162564

Heat stress (HS) in poultry husbandry is an important stressor and with increasing global temperatures its importance will increase. The negative effects of stress on the quality and quantity of poultry production are described in a range of research studies.

heat stress broiler chicken immune system

1. Introduction

Today, heat stress (HS) is increasing in importance due to global warming, and its impacts on poultry production are well known. HS causes performance parameters to deteriorate in both broiler chickens [1] and laying hens [2]. Animal performance is, of course, a determining factor of profitability in poultry husbandry. In recent years, data have been collected, and mechanisms described as to how HS negatively influences weight gain and meat quality in meat-type chickens and disrupts eggshell quality and egg production in laying hens [3][4]. Additionally, HS complicates health management in poultry even as poultry species constitute a rich source of zoonotic diseases [5]. Stress has immunosuppressive potential as a general matter, and many studies in poultry have proven that HS causes dysregulation of the immune system in chickens [6][7][8]. Most negative impacts of HS are associated with oxidative stress, which means the overproduction of reactive oxygen species (ROS) beyond the antioxidant capacity of the organism [9]. The most devastating impacts of oxidative stress occur on the chicken gut, which is the largest area of the body exposed to the environment and the site of most of the immune cells [10]. Therefore, one of the most important factors affecting the poor performance of the chicken under HS conditions is the stimulation of inflammatory processes in the chicken gut [11]. The importance of poultry health management is increasing in today’s world which is endangered by global warming and the coronavirus (COVID-19) pandemic. Therefore, researchers focus on current knowledge of the impacts of heat and oxidative stress on chicken immune cells and lymphoid tissue. However, very little is known about the impacts of HS on individual immune cell phenotypes; therefore, the established effects of heat stress on these cells in chickens are summarized.

2. Impacts of Heat Stress on Cells of the Chicken Immune System

2.1. Dendritic Cells

Dendritic cells are the main presenting cells of the immune system, and they create a connection between innate and adaptive immunity [12]. In an in vitro experiment by Van Goor et al. [13], chicken bone marrow-derived dendritic cells (BMDDC) were stimulated with heat treatment and with lipopolysaccharide (LPS) to evaluate the response of BMDDC to stimulation by those two stressors. LPS induced higher expression of pro-inflammatory cytokines than did heat. Nitric oxide production was also much more pronounced in the LPS-treated group. On the other hand, HSP was strongly induced in BMDDC during heat treatments. The combination of heat treatment with LPS led to the downregulation of LPS-induced inflammation. Additionally, heat treatment downregulated LPS-induced expression of maturation-related genes, such as MHC-II and CD40, in BMDDC. Taken together, results suggest a role of HSP in downregulating inflammatory response stimulated by BMDDS [13]. Furthermore, another important finding is that the heat did not by itself stimulate an inflammatory response in the in vitro culture. Therefore, HS-induced inflammation is a consequence of disrupted gut barrier function due to a flow of inflammation-inducing agents into the organism and those agents’ stimulating inflammation.

2.2. Macrophages

Macrophages are phagocytic cells with antigen-presenting capability. Generally, they are divided into two main subtypes: M1 can rapidly phagocytose and process pathogens; the M2 subtype is responsible for tissue regeneration, such as by transforming into osteoclasts [14]. Chicken macrophages exposed to 45 °C diminished their expression of CCL4, CCL5, IL-1β, IL-8, and inducible nitric oxide synthase below levels seen in the thermoneutral control. On the other hand, HSP expression was highly and significantly expressed in the heat-stressed group. Simultaneous stimulation of macrophages by LPS and heat, by contrast, led to upregulation of pro-inflammatory cytokines IL-1β, IL-8, and inducible nitric oxide synthase [15]. Quinteiro-Filho et al. [16] report that macrophages isolated from the peritoneal cavity of heat-stressed chickens had significantly decreased basal and Staphylococcus aureus-induced oxidative burst. In another study, heat-stressed macrophages in vitro had pronounced lower production of inflammatory mediators due to higher production of anti-inflammatory cytokine IL-10 [17]. Zhang et al. [18] have reported that negative impacts of HS on macrophage function can be seen in osteoclasts. Systemic inflammation caused by HS can stimulate higher numbers and activity of osteoclasts, which in turn cause higher resorption of bone mass and potentially induce skeletal damage in chickens.

2.3. B Lymphocytes

Two major sites of B lymphocytes in birds are the bursa of Fabricius and the spleen. In the bursa of Fabricius, they comprise at least 95% of the entire cell’s population. In the spleen, they are in germinal centers together with follicular dendritic cells and their population makes up less than 20% of the whole organ. During HS, however, both the lymphoid organs tend to decrease in weight. The percentage of B lymphocytes is not influenced by HS in either organ [7]. In peripheral blood, B lymphocytes have been shown to decrease in heat-stressed birds. Additionally, heat treatment early in chickens’ lives decreased the numbers of B lymphocytes in the blood after vaccination against the Newcastle disease virus. However, IgM and IgG levels in the blood increased with heat treatment to levels above those in vaccinated birds. Heat treatment early in chickens’ lives can influence the humoral immune response in the later stages of broiler fattening [19]. Consistently with the just-cited study, Tang and Chen [20] observed significantly decreased numbers of B lymphocytes in peripheral blood and the bursa of Fabricius. IgM, IgG, and IgA levels in the blood were significantly decreased in heat-stressed chickens [20]. Wu et al. [21] also reported their findings that the numbers of proliferating B cells were significantly decreased in peripheral blood during a period of HS. Reduced numbers of B lymphocytes can be explained by structural damage and heat-induced apoptosis in the bursa of Fabricius [22]. Studies of this nature predominantly have described decreasing numbers of B lymphocytes. Consistent with this, many studies have determined lower levels of antibodies because of HS. Mashaly et al. [6] reported that antibody titers in commercial laying hens decreased significantly in a chronically heat-stressed group but not in hens under cyclic HS. Hirakawa et al. [7] found that plasma titers of IgY, IgM, and IgA antibodies against bovine serum albumin were lower in heat-stressed broilers than in thermoneutral control animals. Bartlet and Smith [23] report that primary and secondary antibody response to sheep red blood cells was also negatively affected by HS, and Jahanian and Rasouli [24] published that antibody response against infectious bronchitis virus was diminished by HS in broiler chickens. Experiments have shown that HS causes structural damage to the bursa of Fabricius, a major site of B lymphocytes in chickens, and subsequently decreases their numbers in the blood. Consequently, antibody response to various antigens is disrupted in heat-stressed chickens.

2.4. T Lymphocytes

The thymus is a major site for the development of T lymphocytes; these cells are typically divided into two main subtypes: CD8+ cytotoxic and CD4+ helper T lymphocytes. Mature T lymphocytes are CD3+, but CD3+ T lymphocytes can be found as CD4+CD8+ and CD4−CD8+ and αβ CD4−CD8− and γδ CD4+CD8− subtypes [25]. It is noteworthy that HS has been shown to cause an increased percentage of immature CD4−CD8− and suppression of CD4+CD8+ lymphocytes in the chicken thymus [7]. Several studies have evaluated the effects of HS on CD4 helper and CD8 cytotoxic T lymphocytes. Total T lymphocyte numbers (CD3+) and subtypes CD4 and CD8 increased after a period of HS in the first 6 days of broiler chickens’ lives [19]. When chickens were exposed to HS every day for 2 h, CD3, cytotoxic, and helper T lymphocyte numbers decreased, but CD4 helper T lymphocytes are more affected. Similarly, Jahanian and Rasouli [24] reported that in chickens’ peripheral blood CD4 cells were significantly decreased and CD8 increased in a period of chronic HS. In another study, while HS decreased CD4 and CD8 in the blood of chickens, in the spleen CD4 decreased and CD8 significantly increased. In that same experiment, by Trout and Mashaly [26], other chickens received adrenocorticotropic hormone with almost the same levels of CD4 and CD8. Changes in the composition of T lymphocyte subsets can be explained in part by the effects of stress hormones, and it has been reported that exposure to corticosterone inhibits the proliferation of lymphocytes [27]. However, more studies must be performed to confirm the ways in which HS influences the presence of individual T lymphocyte subtypes.

2.5. Heterophil/Lymphocyte Ratio

Heterophils play a crucial role in innate immunity. Inasmuch as they carry out phagocytosis, these cells represent a mechanism in the first line of immune defense after infection. Heterophils level is a well-known indicator of inflammation, and the H/L ratio is widely used as an indicator of HS. The initial phase of the inflammatory response to HS is accompanied by heterophil activation and their increasing numbers are found in blood. Soleimani et al. [28] proved this response by observing increasing H/L ratio in three different chicken breeds with various levels of susceptibility to HS when exposed to acute HS. In another study, Lee et al. [29] observed an increasing H/L ratio in laying hens exposed through 8 weeks to multiple stress conditions. The H/L ratio has been tested as an indicator for several purposes. In domestic fowl, H/L was identified as an indicator of susceptibility to HS [30]. Additionally, the ratio can be used as a biomarker of susceptibility to Salmonella enteritidis infection in chickens [31]. In a recent study, Wang et al. [32] used a genome-wide profiling technique to identify genes and pathways associated with the regulation of the H/L ratio in chickens. They identified the gene C1QBP as an important candidate gene in regulating the H/L ratio. This gene is involved in protecting cells against oxidative stress-induced apoptosis.

References

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Subjects: Cell Biology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Vladimir Zmrhal
,
Andrea Svoradova
,
Eva Venusova
,
Petr Slama
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Revisions: 2 times (View History)
Update Date: 16 Aug 2023
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