508
A. M. M. Hamdy
Whenever a chick encounters a stressor, the central nervous system first begins to
respond by sending signals to any of the biological systems via behavioral, autonomic
nervous system, neuroendocrine system and immune system in order to alleviate or
compensate the impendence. The response of each chick to a particular stress condition varies depending upon its previous exposure to the stressors, genetic makeup
[67], age [68], season and physiological state. The immune system does not respond
directly to stress but via the neuroendocrine system. The neuroendocrine system
responds mainly to the Hypothalamo—pituitary—Axis (HPA) by the release of glucocorticoids that are normally called as stress hormones [69]. They act to adapt
the chick to cope up with the long-term stressors. The immune system responds to
stress by enhancement or suppression of immune functions [70]. The stress related
hormones act on the immune cell receptors to modulate the immune response.
7 Heat Stress Affecting Chicken Immunity
7.1 Heat Stress Axis
The HPA axis is one of the most important systems for the integration of the body
and is activated in response to stressful stimuli or homeostatic inconvenience [71].
Increased of plasma corticosterone levels may cause consequent deteriorations in
chicken’s health status [44]. It is the thoughtful trunk of the autonomic nervous
system (ANS) arranged in the adrenal medulla. It acts by the arrival of epinephrine
and nor epinephrine which are in charge of the responsible for the characteristic of
flight or -fright mechanism. These hormones act to enhance glycogenolysis causing
increased glucose levels in circulation. The blood glucose will reach the stressed
organ in order to meet the energy requirements and cope up with the stressor [72].
The corticosterone serum levels will be higher when chicks are exposed to
heat. Performance indices deficits and macrophage activity are observed for broiler
stressed chicks. The intestinal integrity might have been a consequence of modifications in HPA function. As a matter of fact, results from Shini et al. [73] indicated that heat exposed chicks caused release in serum corticosterone level. This in
turn increased the heterophil: lymphocyte ratio. Moreover it induced ultrastructural
morphological changes in heterophil size, shape, and granulation and lymphocyte
cytoplasmatic characteristics.
The HPA axis and sympathetic-adrenal-medullary system (SAM) are the crucial
components that receive stress signals and act to relieve the stress mechanism or
adopt the chick to the stressful condition [74]. However, a significant increase in
T3 but not in T4 level was observed during heat stress [75]. During short—term
exposure to high ambient temperature, the concentrations of glucocorticoids and
catecholamines were found to be elevated [76]. Moberg and Mench [24] documented
the simultaneous relationship among thermal stress, plasma aldosterone level and
urine electrolyte concentration. During prolonged heat exposure plasma aldosterone
A. M. M. Hamdy
Whenever a chick encounters a stressor, the central nervous system first begins to
respond by sending signals to any of the biological systems via behavioral, autonomic
nervous system, neuroendocrine system and immune system in order to alleviate or
compensate the impendence. The response of each chick to a particular stress condition varies depending upon its previous exposure to the stressors, genetic makeup
[67], age [68], season and physiological state. The immune system does not respond
directly to stress but via the neuroendocrine system. The neuroendocrine system
responds mainly to the Hypothalamo—pituitary—Axis (HPA) by the release of glucocorticoids that are normally called as stress hormones [69]. They act to adapt
the chick to cope up with the long-term stressors. The immune system responds to
stress by enhancement or suppression of immune functions [70]. The stress related
hormones act on the immune cell receptors to modulate the immune response.
7 Heat Stress Affecting Chicken Immunity
7.1 Heat Stress Axis
The HPA axis is one of the most important systems for the integration of the body
and is activated in response to stressful stimuli or homeostatic inconvenience [71].
Increased of plasma corticosterone levels may cause consequent deteriorations in
chicken’s health status [44]. It is the thoughtful trunk of the autonomic nervous
system (ANS) arranged in the adrenal medulla. It acts by the arrival of epinephrine
and nor epinephrine which are in charge of the responsible for the characteristic of
flight or -fright mechanism. These hormones act to enhance glycogenolysis causing
increased glucose levels in circulation. The blood glucose will reach the stressed
organ in order to meet the energy requirements and cope up with the stressor [72].
The corticosterone serum levels will be higher when chicks are exposed to
heat. Performance indices deficits and macrophage activity are observed for broiler
stressed chicks. The intestinal integrity might have been a consequence of modifications in HPA function. As a matter of fact, results from Shini et al. [73] indicated that heat exposed chicks caused release in serum corticosterone level. This in
turn increased the heterophil: lymphocyte ratio. Moreover it induced ultrastructural
morphological changes in heterophil size, shape, and granulation and lymphocyte
cytoplasmatic characteristics.
The HPA axis and sympathetic-adrenal-medullary system (SAM) are the crucial
components that receive stress signals and act to relieve the stress mechanism or
adopt the chick to the stressful condition [74]. However, a significant increase in
T3 but not in T4 level was observed during heat stress [75]. During short—term
exposure to high ambient temperature, the concentrations of glucocorticoids and
catecholamines were found to be elevated [76]. Moberg and Mench [24] documented
the simultaneous relationship among thermal stress, plasma aldosterone level and
urine electrolyte concentration. During prolonged heat exposure plasma aldosterone