Page 643 - Veterinary Immunology, 10th Edition

stressed, the aggressive ones showed a much greater drop in these
VetBooks.ir responses than the passive animals. Differences in the way animals

cope with stress are thus reflected in differences in immune
reactivity.

The stress effect is mediated by two major pathways. One
involves the autonomic nervous system producing its
neurotransmitters, epinephrine, norepinephrine, and acetylcholine,
and the other is the hypothalamic-pituitary-adrenal cortical axis

producing glucocorticoids. Stress signals the brain to activate these
pathways.

Autonomic Nervous System

Almost all primary and secondary lymphoid organs are supplied

by nerves through the autonomic nervous system, and many cells
of the immune system express receptors for the neurotransmitters
released by both arms of the autonomic nervous system. This may

occur either through adrenergic signals from the sympathetic
nervous system or cholinergic signals from the parasympathetic
nervous system.
The sympathetic nerves act through the neurotransmitter
norepinephrine. They innervate the thymus, the splenic white pulp,

and the lymph nodes. They influence blood flow, vascular
permeability, and lymphocyte migration and differentiation.
Surgical or chemical sympathectomy of the spleen enhances

antibody production and can induce changes in the distribution of
lymphocyte subpopulations. NK cell activity appears to be
modulated directly by the hypothalamus through the splenic nerve.
Autonomic nerves innervate Langerhans cells in the skin. By
releasing neuropeptides, these nerves can depress the antigen-

presenting ability of these cells. This might explain why “hot spots”
in dogs worsen with anxiety. Denervated skin shows reduced
inflammation after tissue damage and heals more slowly. Most

important, sympathetic nerves innervate the adrenal medulla.
Immune cells have a complete set of cholinergic receptors.
Efferent activity in the vagus nerve activates a cholinergic
antiinflammatory pathway. Vagal stimulation suppresses the
systemic response to endotoxin by downregulating hepatic TNF-α

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