Regulation of gene expression in chickens by heat stress.
Goel Akshat,Ncho Chris Major,Choi Yang-Ho
Journal of animal science and biotechnology
High ambient temperatures are a critical challenge in the poultry industry which is a key producer of the animal-based food. To evaluate heat stress levels, various parameters have been used, including growth rates, blood metabolites, and hormones. The most recent advances have explored expression profiling of genes that may play vital roles under stress. A high ambient temperature adversely affects nutrient uptake and is known to modulate the expression of genes encoding for sodium-dependent glucose transporters, glucose transporters, excitatory amino acid transporters, and fatty acid-binding proteins which are responsible for the absorption of macronutrients in the intestine. Various defensive activities are stimulated to protect the cell of different tissues from the heat-generated stress, including expression of early stress response genes coding for heat shock protein (HSP), c-FOS like protein, brain-derived neurotrophic factor (BDNF), and neuronal nitric oxide synthase (nNOS); antioxidant enzyme genes such as superoxide dismutase (SOD), catalase (CAT), and nicotinamide adenine dinucleotide phosphate oxidase (NOX4); and immune-related genes such as cytokines and toll-like receptors (TLRs). The potential role of HSPs in protecting the cell from stress and their presence in several tissues make them suitable markers to be evaluated under heat stress. BDNF and c-FOS genes expressed in the hypothalamus help cells to adapt to an adverse environment. Heat causes damage to the cell by generating reactive oxygen species (ROS). The NOX4 gene is the inducer of ROS under heat stress, which is in turns controlled by antioxidant enzymes such as SOD and CAT. TLRs are responsible for protecting against pathogenic attacks arising from enhanced membrane permeability, and cytokines help in controlling the pathogen and maintaining homeostasis. Thus, the evaluation of nutrient transporters and defense mechanisms using the latest molecular biology tools has made it possible to shed light on the complex cellular mechanism of heat-stressed chickens. As the impacts of heat stress on the above-mentioned aspects are beyond the extent to which the reduced growth performance could be explained, heat stress has more specific effects on the regulation of these genes than previously thought. Effect of heat exposure on the nutrient transporters, antioxidants, and immune inflammation in chickens. Most of the nutrient transporters were suppressed under heat stress. Increase in the production of reactive oxygen species resulted in enhanced production of antioxidant enzymes. Expression of various proinflammatory cytokines and toll-like receptors were enhanced due to heat stress in chicken.
10.1186/s40104-020-00523-5
Hepatic transcriptome profiling according to growth rate reveals acclimation in metabolic regulatory mechanisms to cyclic heat stress in broiler chickens.
Poultry science
Climate change has numerous effects on poultry that result in welfare concerns and economic losses in agricultural industries. However, the mechanisms underlying the acclimation to heat stress in poultry have not been comprehensively defined. Therefore, identifying associated patterns of gene regulation and understanding the molecular mechanisms of acclimation to a warmer environment will provide insights into the acclimation system of broiler chickens. We profiled differentially expressed genes (DEGs) associated with differences in growth performance under heat stress conditions in the liver tissues of broilers based on RNA sequencing data. The DEGs were identified by comparison to the gene expression levels of broilers exhibiting average growth at 28 d of age (D28A) and D36A relative to those at D21A. In D36A, 507 and 312 DEGs were up- and downregulated, respectively, whereas 400 and 156 DEGs were up- and downregulated in D28A, respectively. Pathway enrichment analysis further revealed that "fatty acid degradation" and "heat shock protein expression" were upregulated in broilers exhibiting a higher growth and weight, whereas "cell cycle arrest" and "amino acid metabolism" were downregulated. Transcriptome profiling revealed that the acclimatized group supplied fat and energy from the liver to tissues through the breakdown of fatty acids. Furthermore, homeostasis was maintained via heat shock proteins and antioxidant enzymes. The characterized candidate genes and mechanisms associated with the response to heat stress might serve as a foundation for improving the ability of broilers to acclimatize under heat stress conditions.
10.1016/j.psj.2022.102167
High Temperature-Induced Oxidative Stress Affects Systemic Zinc Homeostasis in Broilers by Regulating Zinc Transporters and Metallothionein in the Liver and Jejunum.
Oxidative medicine and cellular longevity
To investigate the change in zinc homeostasis of broilers under heat stress, 512 broiler chickens were raised to the age of 28 days. The broilers were then assigned to heat stress and normal temperature (36.0°C vs. 26.0°C) groups for 7 days. The results showed that oxidative stress induced by high temperature had a negative effect on the growth performance of broilers. Heat stress altered zinc homeostasis and led to a redistribution of zinc in broilers, which was reflected in increased zinc concentrations in the jejunum, liver, and tibia. Upregulation of the expression of the zinc exporter and importers and in the jejunum indicated that more zinc was absorbed and transported from the jejunum into the blood, while the liver increased its capacity to hold zinc through upregulation of metallothionein () expression, which was achieved by reducing expression and upregulating the expression of the importer . The pathway was mediated by zinc transporters, but the capacity of to chelate and release zinc ions also played a crucial role. The mechanism of alterations in zinc homeostasis under heat stress was revealed by the changes in zinc transporters and levels in the intestine and liver. Heat stress also altered cecal microbial diversity and reduced the relative abundances of and . In conclusion, broilers altered systemic zinc homeostasis through the regulation of zinc transporters and in the liver and jejunum to resist oxidative stress induced by high temperature.
10.1155/2022/1427335
Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver.
Emami Nima K,Jung Usuk,Voy Brynn,Dridi Sami
Antioxidants (Basel, Switzerland)
Lipid metabolism in avian species places unique demands on the liver in comparison to most mammals. The avian liver synthesizes the vast majority of fatty acids that provide energy and support cell membrane synthesis throughout the bird. Egg production intensifies demands to the liver as hepatic lipids are needed to create the yolk. The enzymatic reactions that underlie de novo lipogenesis are energetically demanding and require a precise balance of vitamins and cofactors to proceed efficiently. External stressors such as overnutrition or nutrient deficiency can disrupt this balance and compromise the liver's ability to support metabolic needs. Heat stress is an increasingly prevalent environmental factor that impairs lipid metabolism in the avian liver. The effects of heat stress-induced oxidative stress on hepatic lipid metabolism are of particular concern in modern commercial chickens due to the threat to global poultry production. Chickens are highly vulnerable to heat stress because of their limited capacity to dissipate heat, high metabolic activity, high internal body temperature, and narrow zone of thermal tolerance. Modern lines of both broiler (meat-type) and layer (egg-type) chickens are especially sensitive to heat stress because of the high rates of mitochondrial metabolism. While this oxidative metabolism supports growth and egg production, it also yields oxidative stress that can damage mitochondria, cellular membranes and proteins, making the birds more vulnerable to other stressors in the environment. Studies to date indicate that oxidative and heat stress interact to disrupt hepatic lipid metabolism and compromise performance and well-being in both broilers and layers. The purpose of this review is to summarize the impact of heat stress-induced oxidative stress on lipid metabolism in the avian liver. Recent advances that shed light on molecular mechanisms and potential nutritional/managerial strategies to counteract the negative effects of heat stress-induced oxidative stress to the avian liver are also integrated.
10.3390/antiox10010035
Chronic heat stress promotes liver inflammation in broilers via enhancing NF-κB and NLRP3 signaling pathway.
BMC veterinary research
BACKGROUND:This study investigated the effects of chronic heat stress on liver inflammatory injury and its potential mechanisms in broilers. Chickens were randomly assigned to the 1-week control group (Control 1), 1-week heat stress group (HS1), 2-week control group (Control 2), and a 2-week heat stress group (HS2) with 15 replicates per group. Broilers in the heat stress groups were exposed to heat stress (35 ± 2 °C) for 8 h/d for 7 or 14 consecutive days, and the rest of 26 hours/day were kept at 23 ± 2 °C like control group broilers. Growth performance and liver inflammatory injury were examined for the analysis of liver injury. RESULTS:The results showed that heat stress for 2 weeks decreased the growth performance, reduced the liver weight (P < 0.05) and liver index (P < 0.05), induced obvious bleeding and necrosis points. Liver histological changes found that the heat stress induced the liver infiltration of neutrophils and lymphocytes in broilers. Serum levels of AST and SOD were enhanced in HS1 (P < 0.01, P < 0.05) and HS2 (P < 0.01, P < 0.05) group, compared with control 1 and 2 group broilers. The MDA content in HS1 group was higher than that of in control 1 group broilers (P < 0.05). Both the gene and protein expression levels of HSP70, TLR4 and NF-κB in the liver were significantly enhanced by heat stress. Furthermore, heat stress obviously enhanced the expression of IL-6, TNF-α, NF-κB P65, IκB and their phosphorylated proteins in the livers of broilers. In addition, heat stress promoted the activation of NLRP3 with increased NLRP3, caspase-1 and IL-1β levels. CONCLUSIONS:These results suggested that heat stress can cause liver inflammation via activation of the TLR4-NF-κB and NLRP3 signaling pathways in broilers. With the extension of heat stress time, the effect of heat stress on the increase of NF-κB and NLRP3 signaling pathways tended to slow down.
10.1186/s12917-022-03388-0
Heat stress in broilers of liver injury effects of heat stress on oxidative stress and autophagy in liver of broilers.
Poultry science
This study aimed to investigate the effect of chronic heat stress on oxidative stress in liver of broilers. In our study, chickens were randomly allocated to control 1 group (control 7 d), heat stress 1 group (HS1, 7 d), control 2 group (control 14 d) and heat stress 2 group (HS2, 14 d), with 30 replicates in each group. Broilers in heat stress groups exposed 8 h/day heat stress (35 ± 2°C) for 7 or 14 consecutive days, and the rest of time per day were kept at 23 ± 2℃ the same as control group broilers. Growth performance and the liver tissues were collected for histological observation and detection of organ index and liver redox status. The serum indicators (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) related to liver injury were determined. Moreover, Nrf2-related genes and protein expression levels in liver were measured. The results showed that in heat stress group broilers the body weight gain, feed conversion ratio, liver weight, and liver index were decreased, inflammatory cells infiltration in liver, and serum AST level was enhanced, compared with control group broilers. Moreover, the hepatic malondialdehyde (MDA) and superoxide dismutase (SOD) level were increased after 1 wk of heat stress. Nrf2, Sqstm1/p62, HO-1, and NQO1 mRNA expressions in the liver of broilers were decreased by heat stress. P62 and p-p62 protein expressions were significantly up-regulated, but Nrf2 and keap1 protein level was decreased in heat stress group broilers as compared to control group. The mRNA expression levels of Beclin1, LC3-I, LC3-II were down-regulated significantly with heat stress for 1 wk. The mRNA expression level of mTOR up-regulated after 2 wk of heat stress. In conclusion, heat stress induced liver injury of broilers by down-regulating Nrf2-keap1 signaling pathway and autophagy.
10.1016/j.psj.2022.102085
Integrated transcriptome analysis for the hepatic and jejunal mucosa tissues of broiler chickens raised under heat stress conditions.
Journal of animal science and biotechnology
BACKGROUND:Heat stress (HS) is one of the most important threats for the current poultry industry. Therefore, many efforts have been made to ameliorate the adverse effect of HS on poultry production; however, physiological and molecular mechanisms pertaining to HS are still limited in poultry. Therefore, the objective of the current study was to investigate functional alterations based on individual and integrated transcriptomes in the liver and jejunal mucosa tissues of broiler chickens exposed to HS conditions. RESULTS:Broiler chickens exposed to HS showed decreased growth performance and increased corticosterone concentrations in the feather. In the transcriptome analysis, the number of differentially expressed genes (DEGs) were identified in the liver and jejunal mucosa by HS conditions. In the liver, genes related to amino acid oxidation, tryptophan metabolism, lipid metabolism, oxidative phosphorylation, and immune responses were altered by HS, which support the reason why heat-stressed poultry had decreased productive performance. In the jejunal mucosa, genes related to defense systems, glutathione metabolism, detoxification of xenobiotics, and immune responses were differently expressed by HS conditions. The integrated transcriptome analysis with DEGs found in the liver and jejunal mucosa showed a considerable connectivity between the core nodes in the constructed networks, which includes glutathione metabolism, xenobiotic metabolism, carbon metabolism, and several amino acid metabolisms. CONCLUSIONS:The core network analysis may indicate that increased requirement of energy and amino acids in the jejunal mucosa of broiler chickens exposed to HS conditions is likely compromised by increased oxidation and synthesis of amino acids in the liver. Therefore, our results may provide comprehensive insights for molecular and metabolic alterations of broiler chickens raised under HS conditions, which can aid in the development of the novel strategies to ameliorate the negative effect of HS on poultry productivity and health.
10.1186/s40104-022-00734-y