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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of acute stress on the immune system was examined in mice. Restraint stress decreased the number of lymphocytes in the liver, whereas the number of lymphocytes remained unchanged in the spleen and thymus. In the liver, the decrease in number appeared at 1.5 h and fell to a third of he control level at 3 h. The proportions of IL-2Rbeta(+)CD3(int) cells, NKT cells, CD44(+) T cells and B cells were changed in the liver. The absolute numbers of IL-2Rbeta(+)CD3(int) cells, NKT cells and CD3(+)CD44(+) cells remained constant in the liver under the stress, while those of total T cells and NK cells decreased. The levels of hyaluronan (HA) in various tissues and sera were then examined. The expression of hyaluronan binding protein (HABP) was found to increase in the skin, liver and kidney as shown by immunohistochemical staining. An increase of HA in sera due to stress was seen at 3 h. The present results suggest that the activation of CD44(+) T cells and unconventional T cells (i.e., innate immunity) in the blood and the elevated levels of HA (ligand for CD44) in the tissues and blood are crucial responses to acute stress exposure.
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PMID:Acute stress augments innate immunity in the liver and increases hyaluronan levels in the tissues and blood of mice. 1957 16

It is well-known that acute stress, presumably as a first defense against pathogens, enhances PBMC counts by mobilizing these beta2-adrenoceptor positive cells from the marginal pool. Yet, only select leukocyte subsets participate in this phenomenon of adrenergic leukocytosis and underlying mechanisms are obscure. In this study, we analyzed in human blood adhesion molecule and chemokine receptor profiles in 14 leukocyte subsets, and responsiveness of subsets to epinephrine in vivo and in vitro. Five subsets, namely, CCR7(-)CD45RA(+)CD8(+) effector T cells, CD4(-)CD8(-) gamma/delta T cells, CD3(+)CD56(+) NKT-like cells, CD16(+)CD56(dim) cytotoxic NK cells, and CD14(dim)CD16(+) proinflammatory monocytes showed a rapid and transient increase after infusion of epinephrine at physiological concentrations. These cells were characterized by a CD62L(-)CD11a(bright)CX3CR(bright) phenotype, whereby expression of both CD11a and CX3CR1 was strongly correlated with adrenergic leukocytosis in vivo (r = 0.86 and 0.78, p < 0.005). The same subsets showed highest adherence to activated endothelium in vitro, which (except for proinflammatory monocytes) was reversed by epinephrine. We conclude that these five cytotoxic effector leukocyte subsets comprise the marginal pool by a CD11a/CX3CR1-mediated attachment to the endothelium. Epinephrine rapidly attenuates this attachment to allow demargination and release of the cells into the circulation that, because of their cytotoxic effector function, provide immediate protection from invading pathogens.
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PMID:Selective mobilization of cytotoxic leukocytes by epinephrine. 1994 13