Climatic Change and Chicken Immunity
509
level was reported to decline. Concurrent with this, there was significant fall in serum
K+ [77].
7.2 Hypothalamus—Pituitary—Adrenal Axis (HPA)
The center of pressure reaction is accepted to be founded on the enactment of HPA.
The key segments of this system include: (i) hypothalamus, and (ii) brain stem. The
parvocellular neurons of CRH, arginine vasopressin (AVP) neurons of paraventricular cores of the hypothalamus, CRH neurons of paragigantocellular and parabranchial
nuclei of medulla and locus ceruleus innervate the system [72]. They sense stressor
and get activated to release CRH from the paraventricular nucleus and arginine vasopressin from magnocellular neurons of the hypothalamus. They act on the anterior
pituitary cells to release adrenocorticotropic hormone (ACTH). ACTH, in turn, acts
on adrenal cortex to stimulate synthesis and release of steroids leading to cholesterol
uptake. Cholesterol further gets converted into cortisol and corticosterone. Glucocorticoid receptor exists as a complex in the cytoplasm of most cells including the
immune cells. Glucocorticoid Responsive Elements (GRE), located in the promoter
region of the target gene, regulates the expression of target genes either positively
or negatively. Both conditions are associated with (1) increases in hypothalamicpituitary-adrenal (HPA) axis activity and elevation in serum corticosterone [78], (2)
overall leukocytosis, (3) mild reductions in absolute natural killer (NK) cell counts
and relative T-cell proportions, (4) marginal increases in CD4+ :CD8+ ratios, and
(5) moderate decreases in T-cell and NK-cell function [79].
7.3 The Link Between Stress and the Immune System
Sympathetic innervation from brain connects the primary lymphoid organs and secondary lymphoid organs [80]; thus, the catecholamine receptors in immune cells also
contribute to immune cell activation by stress mechanisms. The end product of HPA
axis activation is glucocorticoid release, which has receptors in almost all organs
including the immune cells [81].
Glucocorticoids increase the transcription of anti- inflammatory cytokines [interleukin (IL)-4 and IL-10] and decrease that of pro inflammatory cytokines (IL-1,
IL-12, IL-6, tumor necrosis factor-α, interferon, and granulocyte macrophage colonystimulating factor) (i.e., they modulate the T-helper type 1 vs. T-helper type 2 cytokine
profile). These hormones decrease the transcription factors for adhesion molecules
such as intercellular adhesion molecule-I and vascular cell adhesion molecule-I [14].
Restraint stress decreases NK cell activity in chickens, most probably due to a transient increase in corticosterone serum levels. Heat stress (39 °C for 7 h/d) presents
509
level was reported to decline. Concurrent with this, there was significant fall in serum
K+ [77].
7.2 Hypothalamus—Pituitary—Adrenal Axis (HPA)
The center of pressure reaction is accepted to be founded on the enactment of HPA.
The key segments of this system include: (i) hypothalamus, and (ii) brain stem. The
parvocellular neurons of CRH, arginine vasopressin (AVP) neurons of paraventricular cores of the hypothalamus, CRH neurons of paragigantocellular and parabranchial
nuclei of medulla and locus ceruleus innervate the system [72]. They sense stressor
and get activated to release CRH from the paraventricular nucleus and arginine vasopressin from magnocellular neurons of the hypothalamus. They act on the anterior
pituitary cells to release adrenocorticotropic hormone (ACTH). ACTH, in turn, acts
on adrenal cortex to stimulate synthesis and release of steroids leading to cholesterol
uptake. Cholesterol further gets converted into cortisol and corticosterone. Glucocorticoid receptor exists as a complex in the cytoplasm of most cells including the
immune cells. Glucocorticoid Responsive Elements (GRE), located in the promoter
region of the target gene, regulates the expression of target genes either positively
or negatively. Both conditions are associated with (1) increases in hypothalamicpituitary-adrenal (HPA) axis activity and elevation in serum corticosterone [78], (2)
overall leukocytosis, (3) mild reductions in absolute natural killer (NK) cell counts
and relative T-cell proportions, (4) marginal increases in CD4+ :CD8+ ratios, and
(5) moderate decreases in T-cell and NK-cell function [79].
7.3 The Link Between Stress and the Immune System
Sympathetic innervation from brain connects the primary lymphoid organs and secondary lymphoid organs [80]; thus, the catecholamine receptors in immune cells also
contribute to immune cell activation by stress mechanisms. The end product of HPA
axis activation is glucocorticoid release, which has receptors in almost all organs
including the immune cells [81].
Glucocorticoids increase the transcription of anti- inflammatory cytokines [interleukin (IL)-4 and IL-10] and decrease that of pro inflammatory cytokines (IL-1,
IL-12, IL-6, tumor necrosis factor-α, interferon, and granulocyte macrophage colonystimulating factor) (i.e., they modulate the T-helper type 1 vs. T-helper type 2 cytokine
profile). These hormones decrease the transcription factors for adhesion molecules
such as intercellular adhesion molecule-I and vascular cell adhesion molecule-I [14].
Restraint stress decreases NK cell activity in chickens, most probably due to a transient increase in corticosterone serum levels. Heat stress (39 °C for 7 h/d) presents