A new Journal of Immunology study suggests that during acute stress the hormone epinephrine (adrenaline) is rapidly causing demargination of cytotoxic effector leukocytes from the marginal pool of blood vessels, thus releasing these cells into the circulation, which, in turn, may provide immediate protection from invading pathogens.
Acute stress in humans is known to cause a rapid and transient leukocytosis.
In the Journal of Immunology study, Dimitrov, Lange and Born demonstrate that an infusion of adrenal medullary hormone epinephrine in healthy human subjects selectively increases the numbers of circulating cytotoxic leukocytes, including effector CD8+ T cells, gamma/delta T cells, NKT-like cells, cytotoxic NK cells, and proinﬂammatory monocytes.
Per the authors, the fast mobilization and recovery of cytotoxic cell counts observed in this and previous studies after stress, exercise, or catecholamine infusion reﬂects the demargination of T cells, NK cells, and monocyte subpopulations.
These effects are caused by adrenal medullary hormone epinephrine binding to beta2-adrenoceptors on peripheral blood mononuclear cells, with high and intermediate levels of beta2-adrenoceptor expression on NK cells and cytotoxic T cells, respectively.
The conditions established in this study mimic those observed during acute stress. In contrast, chronic beta-adrenoceptor stimulation, as addressed in previous studies, may exert opposite effects, with selectively reduced numbers of circulating NK cells and CD8+T cells.
It is concluded that during an acute stress, increased epinephrine release likely serves to selectively recruit cytotoxic effector cells as the first line of defense against pathogens, a mechanism that allows for efficient surveillance of tissues and rapid accumulation at sites of injury and infection.