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Text|Broken Boat Han
Editor|Broken Boat Han
preface
At the beginning of the nineteenth century, Claude Bernard defined stress as a disturbance of the constant state of the "internal environment", and fifty years later, Cannon redefined the concept with the term "homeostasis", defined as "coordinated physiological processes that maintain a steady state in an organism".
Cannon also proposed the "fight or flight response" as the main mechanism by which organisms respond to stress or danger, and experts then expanded the definition of stress to include "the body's non-specific response to any need."
Experts define three stages of general adaptation syndrome (GAS) or biological stress syndrome, the first of which is the identification of toxic substances.
The second stage is resistance or adaptation of the body to stimuli, including the release of secretion granules from the adrenal cortex into the bloodstream that alters tissue metabolism.
This phase is also considered an alarm response, and if stress persists, the last stage is the exhaustion phase, a loss of acquired adaptation and eventually leads to illness.
This definition is important because it incorporates factors of time or duration into the stress response, which is essential for distinguishing between acute and chronic stress.
Pathological phenomena
In the late twentieth century, two experts, McEwan and Goldstein, believed that stress was a conscious or unconscious perceived threat to homeostasis.
Present within a specific range of parameters, the definition recognizes that homeostasis may change over time and vary between individuals in a population.
These changing definitions reveal the difficulty of precisely defining stress responses, which now include broader definitions of fight, flight, or freeze responses.
The factors that cause the stress response are defined as the mental or physical factors perceived in various ways by the organism that disturb the homeostatic state.
But organisms have the ability to initiate complex and coordinated psychological and physiological responses to each stressor, including not only the classic "fight or flight" response, but also the "freeze" response that can immobilize the animal.
In addition, it is recognized that repeated exposure to stress may lead to psychological changes that inhibit, exacerbate or alter the nature of the stress response.
If stress is resolved, then homeostasis can be restored, but if stressors persist or occur repeatedly, then disturbances in homeostasis can lead to psychological and physiological pathologies, from the point of view of livestock production.
These pathologies may manifest as behavioral changes, decreased immune protection affecting disease susceptibility, or metabolic alterations that affect growth, production, or a combination of these responses, and quantifying the effects of stress on animal production can be very difficult, as many of these manifestations can occur at subclinical levels.
Being able to measure stress at the molecular level is essential if there is to be an informed discussion of the effects on animal health, epithesis, and production in terms of specific stressors or combinations of stressors.
In addition, the development of more accurate pressure measurements will enable producers to monitor changes in livestock or production systems and determine whether these changes are reducing or eliminating the physiological effects of acute and chronic stress.
Stress response
Two distinct signaling axes have been identified through which mammals generate an integrated physiological response to perceived hazard, which begins with the release of CRH, and the hypothalamic level of vasopressin.
These hormones transmit signals to the pituitary gland to initiate the release of adrenocorticotropic hormone (ACTH) against the adrenal cortex.
1. Glucocorticoid-induced signaling
Glucocorticoid receptor (GR) is present in the cytoplasm of most cells and is a low-affinity receptor for cortisol, GR is activated by an increase in cortisol concentration after activation of the HPA axis, and glucocorticoid receptor mediates signal transduction through two mechanisms, including genomic and non-genomic effects.
After binding to cortisol, GRs are activated and dissociated from heat shock protein 90 (Hsp90) and Src complexes, activated GR homodimer and transfer from the cytoplasm into the nucleus.
There they can bind to glucocorticoid response elements (GRE), GRE can activate gene expression by enlisting cofactors and histone modifying elements into promoter regions, or GRE can inhibit gene expression by interacting with transcription proteins.
2. Metabolic function activated by glucocorticoid-induced signaling
Glucocorticoids and their receptors serve as checkpoints for energy homeostasis and mediate many stress-related metabolic effects, and studies have shown that carbohydrate metabolism is regulated under heat stress, resulting in decreased leukocyte metabolism in peripheral blood of bovines.
Altered expression of kinase genes involved in glycolysis and insulin-induced glucose uptake following bovine heat stress treatment has also been reported, and further research is needed to determine whether these metabolic responses are specific to heat stress.
Glucocorticoid receptors, which also play an important role in regulating the balance between anabolism and catabolism.
GRα, a subtype of the glucocorticoid receptor, has been shown to silence and activate the expression of transcription factor 4 (ATF4), a transcription factor involved in amino acid biosynthetase.
This further suggests that glucocorticoids play an important role in regulating anabolism and catabolism, and that lipoprotein lipase (LPL) activity is also reduced after glucocorticoid-induced lipolysis of adipose tissue, so glucocorticoids can regulate a wide range of metabolic functions.
Biological function is regulated by two stress axes
3. Glucocorticoid-induced signaling-regulated immune response
Corticosteroids can affect a wide range of innate and acquired immune responses, such as glucocorticoids with anti-inflammatory effects.
However, a recent study suggests that glucocorticoids can also induce a pro-inflammatory response, consistent with expert studies that determined that maternal isolation and binding to transport increases postviral interferon (IFN)-γ secretion and enhances protein production in the acute phase.
Glucocorticoids can also enhance innate immune responses by increasing the expression and signaling of TLRs, and the media reported that individual stressors had significantly different effects when bovine blood mononuclear cells measured LPS-induced TLR4 signaling.
LPS-induced increase in tumor necrosis factor (TNF) secretion was significantly greater in solitary transport calves than in calves that endured a combined stressor of transport and sudden weaning.
Although induction of elevated serum cortisol is similar, the effects of specific stressors on innate immune responses may differ significantly.
Glucocorticoids can inhibit the expression of pro-inflammatory genes through the interaction of GR with transcription factors, and a variety of other regulatory proteins may also mediate the anti-inflammatory effects of glucocorticoids.
Glucocorticoids, inhibition of p38 mitogen-activated protein kinase (MAPK), are mediated by MAPK phosphatase-1.
In vitro glucocorticoid effect analysis, which contradicts endogenous cortisol during stress response, after elevation, suggests that the regulation of cell signaling may be much more complex in vivo.
Unraveling this apparent contradiction may require new methods to analyze the cellular signaling responses initiated under the combined influence of the HPA and SAM axes.
Glucocorticoids have been reported to have a variety of effects on the acquired immune response, which may include altered lymphocyte transport, naïve lymphocyte apoptosis, regulation of cytokine secretion, reduction of the proportion of helper/suppressor T cells, and reduction of antibody production.
The extent, duration, and timing of cortisolaemia elevation required to influence significant changes in the acquired immune response remains to be determined.
4. Catecholamine signaling
Norepinephrine and epinephrine, two catecholamine neurotransmitters released by the SAM axis, act through α and β adrenergic receptors, but mainly beta2-adrenergic receptors, and this interaction affects a variety of body systems.
Increases heart rate, blood pressure, respiratory rate, and decreases gastrointestinal activity, these combined physiological changes are part of the observed response after acute stressors.
At the cellular level, β-adrenergic receptors signal via G proteins, which catalyze cAMP synthesis, activate cAMP-dependent protein kinase A (PKA) and transcription factors involved in regulating gene expression.
5. Metabolic function of catecholamine-induced signal activation
Epinephrine affects glucose metabolism through two mechanisms, first, through transcription factor activation mediated by the protein kinase AMPK.
The coactivator peroxisome proliferator-activated receptor γ coactivator 1α, which stimulates mitochondrial biogenesis, which leads to an increase in glucose metabolism.
Another mechanism is that insulin and AMPK work together to increase the glucose transporter GLUT4 and transfer GLUT4 to the cell membrane, leading to increased glucose uptake by cells, catecholamines may also affect insulin signaling, lipid metabolism, and thermogenesis.
6. Catecholamine-induced signaling-regulated immune response
Catecholamines have also been implicated in alterations in various immune functions, with epinephrine reported to inhibit wound epithelialization, alter neutrophil trafficking, regulate cytokine secretion, and alter host-pathogen interactions by altering microbial growth.
Treatment with reserpine, a type of indolol, reduces the level of circulating norepinephrine and increases the level of TNF-α.
In addition, increasing the concentration of circulating norepinephrine can reduce the LPS-induced response and play a large role in regulating cytokine production.
Epinephrine released from keratinocytes can also bind to β2-adrenergic receptors in an autocrine manner and induce activation of the AKT signaling pathway.
This signaling stabilizes the cytoskeleton, increases focal adhesion formation, and ultimately inhibits keratinocytes migration, and these epinephrine-induced changes in epithelial cell function can lead to impaired wound healing.
Stressors studied in cattle
Research related to stress across all species has increased dramatically over the past 20 years, with more than 1,000 citations in 50 years.
In contrast, research activity related to cattle stress has remained relatively stable, with fewer than 4 citations per year over the past 50 years.
These account for less than 1% of all stress-related studies, and studies related to stress and disease account for nearly 25% of current cattle stress-related research, but stress- and behavior-related studies account for less than 10% of cattle stress-related studies.
Over the past 50 years, many stressors have been studied in cattle, which can be classified as physical or psychological.
These are convenient categories for stress classification, but in normal animal husbandry practice, cattle experience many stressors at the same time.
This complicates the investigation of a possible link between stress and declining animal production or health, which the researchers try to simplify by subjecting animals to a single, controlled stress.
But these studies may be complicated by monitoring animal-related stress effects during the study period, and will be used to study the range of stressors and model systems of bovine stress biological effects, but acknowledges that many studies are complicated by exposure to multiple stressors, including those associated with sample collection.
Number of publication entries in Medline (PubMed) Trends* from 1995 to 2013
conclusion
The definition of stress has evolved to recognize that individual animal responses vary widely and that physiological responses to stress change rapidly over time.
Others have individual animals where repeated exposure to specific stresses may lead to adaptation to stress or promote enhanced stress responses.
The challenge now for those involved in animal husbandry is to accurately assess how individual animals respond to potentially stressful situations and determine whether homeostasis is severely disturbed, which experts have highlighted as homeostatic disturbances, which have been measured in terms of altered metabolism and immune function.
Emerging approaches that then affect the health, well-being, and productivity of animals, emerging areas of immune metabolism provide a framework for more integrated analysis of stress responses.
Not only do these techniques provide a more comprehensive picture of physiological responses, but their high throughput capabilities make it possible to analyze dynamic changes over time, and the question remains as to how these techniques will be applied to improve the potential negative effects of stress in animals.
They certainly contribute to better definition, biological effects of single or combined stressors, and to determining the duration of physiological disturbances after exposure to acute and chronic stressors.
A more controversial area may be the application of the knowledge provided by these techniques to the development of stress suppression therapies or genetic selection in animals.
If drugs can be used to suppress physiological responses that negatively affect animal health, or production, is it appropriate to ignore stressful animal production or handling systems?
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