Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we investigated whether restraint stress induces either apoptotic cell death or lymphocyte migration in Peyer's patches. Exposure to stress induced a striking decrease in the number of CD3+CD4+, CD3+CD8+ and B220+ cells. Such decreases were accompanied by the enhanced induction of apoptosis in Peyer's patches. The apoptosis of Peyer's patch cells was completely reversed by pretreatment with either high or low doses of RU-486, a glucocorticoid receptor antagonist. In contrast, the stress-induced lymphopenia was little affected by administration of low doses of RU-486, although such lymphopenia was perfectly inhibited by treatment with high doses of RU-486. Taken together, these results suggest that the stress-induced lymphopenia in Peyer's patches is partly due to apoptotic cell death, although other systems such as lymphocyte migration, may contribute to such a reduction in the number of Peyer's patch cells.
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PMID:Restraint stress-induced elevation of endogenous glucocorticoids decreases Peyer's patch cell numbers via mechanisms that are either dependent or independent on apoptotic cell death. 1204 61

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1alpha/CXCL12. Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.
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PMID:Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress. 1552 95