engleski

PTSD as a model of neuroendocrine-immune interactions

The stress response can be considered as a study model for neuroendocrine-immune interactions. Distinct profile of hypothalamic-pituitary-adrenocortical (HPA) axis, manifested by low cortisol level and increased number of glucocorticoid receptors (GR), is considered to be characteristic of posttraumatic stress disorder (PTSD). The findings mainly rely on studies performed decades following exposure to trauma. The purpose of this study was to evaluate the effect of combat-associated traumatic experience on hormonal and immune responses in war veterans with PTSD diagnosed by DSM-IV two years after exposure. Participants were 32 PTSD sufferers and age matched civilian controls. Serum hormone (cortisol, prolactin, T3, T4) and cytokine (IL-1 , IL-6, TNF- , IFN- ) levels were determined by radio- and enzyme immunoassays. The absolute number and proportions of total T, B and NK cells, helper and cytotoxic lymphocytes, CD4 memory and activated B cell subpopulations were determined by flow cytometry. Phagocytic functions (ingestion, digestion, ADCC), and NK cell activity were measured by 51Cr-release assays. GR expression was determined by flow cytometry by intracellular staining with  -GR (5E4-B1), and evaluated as relative fluorescence intensity (r.f.i.). Serum levels of TNF- , IL-6 and prolactin were increased while T4 level was decreased in PTSD. The total lymphocyte and CD3, CD4, CD8 and CD45RO absolute counts were increased. Although the number of NK cells in PTSD did not differ from controls, their cytotoxicity was enhanced but phagocytic functions, cortisol, T3, IL-1 and IFN- levels were not affected. GR expression were lower in monocytes, lymphocytes, CD3, CD4, and NK cells. A negative correlation was found between cortisol level and GR expression, while prolactin level was in positive correlation with NK activity. In early stages of PTSD studied (two years after exposure), HPA axis seem to be activated rather than suppressed. This activation could lead to the enhanced negative feedback inhibition described in late PTSD.

cortisol; prolactin; T3; T4; proinflammatory cytokines; glucocorticoid receptors; NK activity; Phagocytic activity; immunophenotyping

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