Intestinal Barrier Integrity in Heat-Stressed Modern Broilers and Their Ancestor Wild Jungle Fowl

Tabler, Travis W.; Greene, Elizabeth S.; Orlowski, Sara; Hiltz, J.Z.; Anthony, Nicholas B.; Dridi, Sami

doi:10.3389/fvets.2020.00249

Cited by 60 publications

(87 citation statements)

References 49 publications

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“…Furthermore, heat stress reduces the activity of digestive enzymes such as amylase, maltase, lipase, trypsin, and chymotrypsin, which in turn results in reduced dietary digestibility [ 52 ]. In addition, heat stress induces mucosal lesions in the small intestine and leaky gut syndrome [ 53 , 54 ]. Comparison of low and high feed efficient broilers showed higher production of H 2 O 2 and protein carbonyls in the liver of low feed efficient broilers [ 55 ].…”

Section: Heat Stress and Oxidative Stress In Commercial Poultry—a mentioning

confidence: 99%

Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver

et al. 2020

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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.

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Section: Heat Stress and Oxidative Stress In Commercial Poultry—a mentioning

confidence: 99%

Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver

et al. 2020

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“…Damage to the intestinal mucosa leads to decreased feed efficiency, and suppressed nutrient transporters and immune responses, and subsequently facilitates luminal bacteria translocation and impairs growth performance [ 38 ]. Drastic consequences of heat stress were found in intestinal segments’ pathological injuries, mainly epithelium integrity and villus structure [ 39 , 40 ]. Exposure to high temperatures causes several defects in the intestinal epithelium, including damage to villus length and tip integrity, and increased cell shedding, which is thought to reduce epithelial barrier functions and increase vulnerability to bacterial translocation [ 39 , 41 ].…”

Section: Heat Stressmentioning

confidence: 99%

“…Drastic consequences of heat stress were found in intestinal segments’ pathological injuries, mainly epithelium integrity and villus structure [ 39 , 40 ]. Exposure to high temperatures causes several defects in the intestinal epithelium, including damage to villus length and tip integrity, and increased cell shedding, which is thought to reduce epithelial barrier functions and increase vulnerability to bacterial translocation [ 39 , 41 ]. Heat stress induces apoptosis in intestinal epithelial cells by accumulated ROS and activates the lysosomal–mitochondrial apoptotic pathway which is involved in triggering cathepsin-B release [ 42 ].…”

Section: Heat Stressmentioning

confidence: 99%

“…Hosseindoust et al [ 168 ] reported that the level of HSP70 was significantly upregulated in different sections of the small intestine of chicken under acute heat stress. However, the expression of HSP family members in intestinal segments differs between genotypes under heat-stress conditions [ 39 ]. HSP70 preserves the intestinal mucosa from heat-stress-induced injuries by enhancing antioxidant capacity, preventing lipid peroxidation, minimizing cell damage, and controlling the production of lactic dehydrogenase ( Figure 3 ) [ 43 ].…”

Section: Cytoprotective Role Of Hsps Against Heat-stress-induced Imentioning

confidence: 99%

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Modulation of Heat-Shock Proteins Mediates Chicken Cell Survival against Thermal Stress

Shehata

Saadeldin

Tukur

et al. 2020

Animals

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Heat stress is one of the most challenging environmental stresses affecting domestic animal production, particularly commercial poultry, subsequently causing severe yearly economic losses. Heat stress, a major source of oxidative stress, stimulates mitochondrial oxidative stress and cell dysfunction, leading to cell damage and apoptosis. Cell survival under stress conditions needs urgent response mechanisms and the consequent effective reinitiation of cell functions following stress mitigation. Exposure of cells to heat-stress conditions induces molecules that are ready for mediating cell death and survival signals, and for supporting the cell’s tolerance and/or recovery from damage. Heat-shock proteins (HSPs) confer cell protection against heat stress via different mechanisms, including developing thermotolerance, modulating apoptotic and antiapoptotic signaling pathways, and regulating cellular redox conditions. These functions mainly depend on the capacity of HSPs to work as molecular chaperones and to inhibit the aggregation of non-native and misfolded proteins. This review sheds light on the key factors in heat-shock responses for protection against cell damage induced by heat stress in chicken.

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“…For example, heat stress is one of the stressors that greatly affect productivity in the chicken industry. It deteriorates gut physiology, causing leaky gut syndrome by reducing the expression of tight junction proteins [ 49 ]. In addition, it reduces the development of lymphoid organs, thereby reducing T and B cells and impairing humoral immunity against antigens [ 50 ].…”

Section: Stressors and Immune Responsementioning

confidence: 99%

Immunosecurity: immunomodulants enhance immune responses in chickens

Choi

Yun

2021

Anim Biosci

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The global population has increased with swift urbanization in developing countries, and it is likely to result in a high demand for animal-derived protein-rich foods. Animal farming has been constantly affected by various stressful conditions, which can be categorized into physical, environmental, nutritional, and biological factors. Such conditions could be exacerbated by banning on the use of antibiotics as a growth promoter together with a pandemic situation including, but not limited to, African swine fever, avian influenza, and foot-and-mouth disease. To alleviate these pervasive tension, various immunomodulants have been suggested as alternatives for antibiotics. Various studies have investigated how stressors (i.e., imbalanced nutrition, dysbiosis, and disease) could negatively affect nutritional physiology in chickens. Importantly, the immune system is critical for host protective activity against pathogens, but at the same time excessive immune responses negatively affect its productivity. Yet, comprehensive review articles addressing the impact of such stress factors on the immune system of chickens are scarce. In this review, we categorize these stressors and their effects on the immune system of chickens and attempt to provide immunomodulants which can be a solution to the aforementioned problems facing the chicken industry.

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Intestinal Barrier Integrity in Heat-Stressed Modern Broilers and Their Ancestor Wild Jungle Fowl

Cited by 60 publications

References 49 publications

Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver

Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver

Modulation of Heat-Shock Proteins Mediates Chicken Cell Survival against Thermal Stress

Immunosecurity: immunomodulants enhance immune responses in chickens

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