摘要：热应激组的鸡肺组织表现出不同程度的充血和出血。在28龄时，HS组的肺组织中细胞间距增加，炎症细胞浸润明显。在35和42日龄时，HS组鸡的肺组织中大量上皮细胞脱落，微血管的内皮结构受损，红细胞显著增加。

热应激对肠道健康的影响

肠道上皮膜由通过粘附连接（AJ）、紧密连接（TJ）和桥粒紧密相连的上皮细胞构成。负责营养物质的运输，并作为抵御病原物质的天然防御屏障。

热应激会不利地影响肠粘膜中的紧密连接，导致由于肠漏引起的病原体渗透。病原体进入激活的促炎细胞因子进一步导致免疫炎症。

热应激对鸡肺脏的影响

热应激组的鸡肺组织表现出不同程度的充血和出血。在28龄时，HS组的肺组织中细胞间距增加，炎症细胞浸润明显。在35和42日龄时，HS组鸡的肺组织中大量上皮细胞脱落，微血管的内皮结构受损，红细胞显著增加。

热应激对产蛋鸡体重、免疫器官的影响

产蛋鸡的平均体重在对照组在整个期间内变化不大（P > 0.05），而热应激组在暴露至30天时，平均体重持续下降（P

INTRODUCTION During the twenty-first century, climate change is expected to cause worldwide elevated temperatures, with the current UN Climate Change Report (2023) indicating that elevated temperature extremes during heat waves are “virtually certain (99–100% probability)” (1). These extreme temperatures will adversely influence food production, in particular production of animal protein. Worldwide, poultry has become the largest source of animal protein. In 2022, the top 10 countries produced approximately 17 billion chickens, yielding 112 million tons of meat and 1.2 trillion eggs. By 2100, the world population is expected to exceed 10 billion, and providing food security for this population will require increasing poultry production. One impact of climate change on poultry will be heat stress that will cause production losses due mortality and morbidity. In addition to pathology directly induced by heat, heat stress also causes immunosuppression in both broilers and layers , leaving them more susceptible to infectious pathogens. Climate change is expected to shift ranges of pathogens and potentially result in a new era of emerging, reemerging, and endemic pathogens . Heat stress occurs when the internal temperature exceeds the organism’s thermoneutral zone— the range of temperature in which the organism does not need to expend extra energy to regulate its body temperature. For chickens, the thermoneutral zone is between 18°C and 24°C , and once the temperature exceeds 27°C, the birds need to reduce their heat burden. Many responses that improve the bird’s chances of surviving heat stress reduce meat and egg production. Sensing heat stress in vertebrates begins with the activation of transient receptor potential cation channels in peripheral tissues. These sensory data are transmitted to the parabrachial nucleus of the brain stem via the spinal cord. This nucleus conveys temperature information to the preoptic area of the hypothalamus, which then signals other physiological systems (Figure 1). The signals lead to various responses, including reduced feed intake, reduced movement, panting, wing spreading, and increased drinking. Another response directed from the preoptic area is increased skin vasodilation that diverts blood to the skin and improves heat loss. Vasodilation, along with visceral vasoconstriction, occurs particularly in the intestine. The vasoconstriction is significant, because it can lead to loss of intestinal tight junction integrity, with subsequent leaking of bacterial toxins into the bloodstream (5). This “leaky” gut can then lead to systemic inflammatory responses.

The hypothalamus also releases corticotropin-releasing hormone,1 directing the pituitary to release adrenocorticotropin. Subsequently, the adrenocorticotropin acts on the adrenal glands to promote release of corticosterone, resulting in various responses including decreased fecundity and immune function along with elevated plasma levels of glucose, fatty acids, and amino acids. At the cellular level, heat stress leads to uncoupling of the electron transport chain to reduce heat production, but this results in increased levels of reactive oxygenspecies (ROS) that can cause cellular damage. At the molecular level, heat stress leads to protein denaturation and misfolding. This can inhibit many cellular processes, including proliferation,signal transduction,membrane structure, translation, and vesicle transport. In addition, the production of ROS, which can oxidize cellular components including DNA, proteins (8), and lipids (9), results in an increased mutation rate, modification of protein function, and altered membrane properties. If damage is sufficient, cell death pathways are activated, leading to apoptosis or necrosis.

来源：鸡保姆