Heat stress (HS) is one of the most important stressors in chickens, and its adverse effects are primarily caused by disturbing the redox homeostasis. An increase in electron leakage from the mitochondrial electron transport chain is the major source of free radical production under HS, which triggers other enzymatic systems to generate more radicals. As a defense mechanism, cells have enzymatic and non-enzymatic antioxidant systems that work cooperatively against free radicals. The generation of free radicals, particularly the reactive oxygen species (ROS) and reactive nitrogen species (RNS), under HS condition outweighs the cellular antioxidant capacity, resulting in oxidative damage to macromolecules, including lipids, carbohydrates, proteins, and DNA. Understanding these detrimental oxidative processes and protective defense mechanisms is important in developing mitigation strategies against HS. This review summarizes the current understanding of major oxidative and antioxidant systems and their molecular mechanisms in generating or neutralizing the ROS/RNS. Importantly, this review explores the potential mechanisms that lead to the development of oxidative stress in heat-stressed chickens, highlighting their unique behavioral and physiological responses against thermal stress. Further, we summarize the major findings associated with these oxidative and antioxidant mechanisms in chickens.

Glucose level in birds’ tissue decreases due to heat stress (HS)-induced reduction in feed intake (FI); impairing metabolism and growth. The effect of glucose supplementation on the performance of broiler chickens was evaluated under thermoneutral (TN) and HS conditions. Glucose was supplemented at 0 and 6% under TN-(25 °C) and HS-(25 °C–35 °C–25 °C) conditions. The treatments were TN + 0%-glucose (TN0); TN + 6%-glucose (TN6), HS + 0%-glucose (HS0) and HS + 6%-glucose (HS6). There were 6 replicates (19 birds each)/treatment. Heat and glucose supplementation were applied from d28–35. At d35, Pectoralis (P.) major was sampled from one bird/replicate to determine glucose transporters’ mRNA expression. Heat application lowered (p < 0.05) FI, body weight gain, and increased feed and water conversion ratios. Glucose supplementation increased total energy intake by 4.9 and 3.2% in TN and HS groups, respectively but reduced FI under TN and HS conditions. The P. major- and drumstick-yield reduced (p < 0.05) in HS0 compared to TN0, TN6 and HS6. Under HS, glucose supplementation improved eviscerated carcass weight by 9% and P. major yield by 14%. Glucose supplementation increased SGLT1 expression with/without heat treatment while HS independently increased the expression of GLUT 1, 5 and 10. Glucose supplementation under HS could improve performance of broilers.

Reduced feed intake during heat stress (HS) disrupts glucose homeostasis, thereby resulting in endoplasmic reticulum (ER) stress and triggering apoptosis in chickens. We hypothesize that glucose supplementation could reduce apoptosis in chickens raised under HS. This study comprised 456 28-day-old broiler chickens randomly assigned to four treatment combinations under glucose supplementation and HS. The treatments were TN₀, TN₆, HS₀, and HS₆ with two glucose levels (0% and 6%) and two temperature levels (25 °C (thermoneutral-TN) and 35 °C (8.00 AM to 8.00 PM, (HS)). After 7 days post-HS, the blood glucose level for the HS₆ group was higher than for TN₀, TN₆, and HS₀. We studied the mRNA expression of genes and caspase-3 activity in the four experimental groups. The expressions of GCN2, ATF4, CHOP, and FOXO3a increased during HS regardless of glucose supplementation, while PERK and MAFbx increased only under HS with glucose supplementation. We show that under TN conditions, glucose supplementation led to a significant increase in cellular apoptosis in the Pectoralis (P.) major. However, under HS with glucose, the level of apoptosis was similar to that of chickens raised under TN conditions with no glucose supplementation. The utility of glucose to curtail apoptosis under HS should be tested under other intense models of HS.

Porcine deltacoronavirus (PDCoV) is an emerging enteric pathogen in pigs and a newly recognized zoonotic coronavirus in humans. Genetic analyses suggest that PDCoV originated from avian deltacoronaviruses, with sparrow deltacoronaviruses (SpDCoVs) being the most closely related. House sparrows (Passer domesticus) frequently visit farms and interact directly with pigs in barns, raising the possibility of interspecies transmission. We hypothesized that PDCoV can be transmitted between pigs and house sparrows. To investigate this, 200 house sparrows near Ohio swine farms were sampled and screened for gammacoronaviruses and deltacoronaviruses using RT-PCR targeting the conserved RNA polymerase region. Deltacoronaviruses and gammacoronaviruses were detected in 18.0% (36/200) and 5.5% (11/200) of fecal samples, respectively. Genomic sequence analysis of representative samples revealed that SpDCoVs are closely related to, but not direct ancestors of, PDCoVs. These SpDCoVs appear to be widespread in the U.S. Midwest and may contribute to PDCoV evolution. Attempts to isolate SpDCoV from these samples in embryonated chicken eggs and four cell lines were unsuccessful. Because coronaviruses frequently cross species barriers to cause epidemics and/or pandemics in humans and livestock, these findings underscore the need for ongoing surveillance of deltacoronaviruses in diverse wild animals, livestock, and humans to safeguard public health.

Porcine deltacoronavirus (PDCoV) is an emerging enteric pathogen in pigs and a newly recognized zoonotic coronavirus in humans. Genetic analyses suggest that PDCoV origi-nated from avian deltacoronaviruses, with sparrow deltacoronaviruses (SpDCoVs) being the most closely related. House sparrows (Passer domesticus) frequently visit farms and in-teract directly with pigs in barns, raising the possibility of interspecies transmission. We hypothesized that PDCoV can be transmitted between pigs and house sparrows. To inves-tigate this, 200 house sparrows near Ohio swine farms were sampled and screened for gamma- and deltacoronaviruses using RT-PCR targeting the conserved RNA polymerase region. Deltacoronaviruses and gammacoronaviruses were detected in 18.0% (36/200) and 5.5% (11/200) of fecal samples, respectively. Genomic sequence analysis of representative samples revealed that SpDCoVs are closely related to, but not the direct ancestors of, PDCoVs. These SpDCoVs appear to be widespread in the U.S. Midwest and may contrib-ute to PDCoV evolution. Attempts to isolate SpDCoV from these samples in embryonated chicken eggs and four cell lines were unsuccessful. Because coronaviruses frequently cross species barriers to cause epidemics and/or pandemics in humans and livestock, these findings underscore the need for ongoing surveillance of deltacoronaviruses in diverse wild animals, livestock, and humans to safeguard public health.