510
A. M. M. Hamdy
decreased CD4+ and CD8+ cells and SRBC antibody titers in chickens [82]. Injection of corticosterone decreases antibody production against SRBC and impaired
bronchitis vaccine response in chickens [83].
7.4 Heat Stress and Innate Immunity
This refers to the natural or inherited ability to resist disease and the involved mechanisms that come into play immediately after a few hours that an antigen has appeared
in the body. However, it is possible that specifically through corticosterone release;
heat stress could decrease the chickens’ innate immune response in commercial
industrial production, thus decreasing their resistance to other pathogens, such as
coccidia. Altogether, the central nervous system activation by heat stress is responsible for the changes in intestinal immunity, which reinforces the idea of the existence of
a link between the nervous and immune systems in maintaining intestinal homeostasis. Included in this type of immunity are a number of non-specific disease response
mechanisms. Concerning the effects of heat stress on avian species, the following
findings were reported: (1) decreases in the feed consumption, BW gain, as well as
the total white blood cell count and antibody production [41]; (2) decreases in the
number of peripheral blood lymphocytes and induction of an electrolyte imbalance
[48]; (3) decreases in the blood lymphocytes and spleen weight [84]; (4) decreases
in CD4+ and CD8+ lymphocytes and antibody production against SRBC [82] and
(5) decreases in the wet and dry weights of jejunum [85].
7.5 Heat Stress and Adaptive Immunity
Adaptive immunity creates “immunological memory” once an initial response to a
specific pathogen has been triggered, which can enhance future responses to that specific pathogen and act more efficiently. These antigen-specific immune responses are
provided by immune cells or antibodies that are produced in response to exposure to
an antigen. These antibodies are very small, very special proteins (globulin proteins)
that chickens release into their circulatory system, which fight foreign invaders e.g.
invading viruses and bacteria [14].
The adaptive immunity is specific to an antigen and can take one of two forms:
a-Antibodies: Antibodies do not have the capability to kill disease organisms
directly. Antibodies perform their function by attaching to disease organisms and
blocking their receptors. The disease organisms are then prevented from attaching to
their target cell receptors in the chicken. The attached antibodies also immobilize the
disease organism which assists their destruction by macrophages’. b-The cellular
immune response: The cell segment of the resistant reaction incorporates every one
of the cells that respond with specificity to antigens, aside from those related with
counter acting agent generation. The cells related with this system, the T-lymphocytes
A. M. M. Hamdy
decreased CD4+ and CD8+ cells and SRBC antibody titers in chickens [82]. Injection of corticosterone decreases antibody production against SRBC and impaired
bronchitis vaccine response in chickens [83].
7.4 Heat Stress and Innate Immunity
This refers to the natural or inherited ability to resist disease and the involved mechanisms that come into play immediately after a few hours that an antigen has appeared
in the body. However, it is possible that specifically through corticosterone release;
heat stress could decrease the chickens’ innate immune response in commercial
industrial production, thus decreasing their resistance to other pathogens, such as
coccidia. Altogether, the central nervous system activation by heat stress is responsible for the changes in intestinal immunity, which reinforces the idea of the existence of
a link between the nervous and immune systems in maintaining intestinal homeostasis. Included in this type of immunity are a number of non-specific disease response
mechanisms. Concerning the effects of heat stress on avian species, the following
findings were reported: (1) decreases in the feed consumption, BW gain, as well as
the total white blood cell count and antibody production [41]; (2) decreases in the
number of peripheral blood lymphocytes and induction of an electrolyte imbalance
[48]; (3) decreases in the blood lymphocytes and spleen weight [84]; (4) decreases
in CD4+ and CD8+ lymphocytes and antibody production against SRBC [82] and
(5) decreases in the wet and dry weights of jejunum [85].
7.5 Heat Stress and Adaptive Immunity
Adaptive immunity creates “immunological memory” once an initial response to a
specific pathogen has been triggered, which can enhance future responses to that specific pathogen and act more efficiently. These antigen-specific immune responses are
provided by immune cells or antibodies that are produced in response to exposure to
an antigen. These antibodies are very small, very special proteins (globulin proteins)
that chickens release into their circulatory system, which fight foreign invaders e.g.
invading viruses and bacteria [14].
The adaptive immunity is specific to an antigen and can take one of two forms:
a-Antibodies: Antibodies do not have the capability to kill disease organisms
directly. Antibodies perform their function by attaching to disease organisms and
blocking their receptors. The disease organisms are then prevented from attaching to
their target cell receptors in the chicken. The attached antibodies also immobilize the
disease organism which assists their destruction by macrophages’. b-The cellular
immune response: The cell segment of the resistant reaction incorporates every one
of the cells that respond with specificity to antigens, aside from those related with
counter acting agent generation. The cells related with this system, the T-lymphocytes