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No response of plasma substance P, but delayed increase of interleukin-1 receptor antagonist to acute psychosocial stress.
Life Sci. 2006 May 22; 78(26):3082-9.LS

Abstract

Psychosocial stress has been shown to induce inflammatory reactions, followed by the release of immunosuppressive glucocorticoids. This may be mediated by catecholamines or other stress reactive substances such as neuropeptides or cytokines. We here set out to explore the effects of acute psychosocial stress on plasma levels of substance P (SP), a possible mediator of stress-induced inflammatory reactions, and interleukin-1 receptor antagonist (IL-1ra). Twelve healthy male subjects (mean age 27 yrs.) were subjected to the psychosocial stress test "Trier Social Stress Test" (TSST) and a resting control condition. Blood and saliva samples were taken before, as well as 1, 20, 45, and 90 min after TSST or rest, respectively. Salivary cortisol and plasma SP and IL-1ra were measured using immunoassays, salivary alpha-amylase (sAA) was measured by an enzyme kinetic method, and plasma epinephrine (E) and norepinephrine (NE) were measured by HPLC. The TSST induced immediate increases of E, NE, and sAA, and a delayed increase of free cortisol. Plasma IL-1ra showed an even further delayed peak at 90 min after stress. Plasma levels of SP did not respond to stress. No significant associations between changes of stress hormones and IL-1ra or SP were found. We conclude that substance P, epinephrine, and norepinephrine are probably not involved in mediating peripheral inflammation following psychosocial stress, at least with respect to IL-1ra. Further studies have to reveal the mechanisms involved in the stress-induced up regulation of IL-1ra.

Authors+Show Affiliations

Department of Psychology, Dresden University of Technology, Zellescher Weg 17, D-01069 Dresden, Germany. nicolas.rohleder@biopsych.tu-dresden.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16414081

Citation

Rohleder, Nicolas, et al. "No Response of Plasma Substance P, but Delayed Increase of Interleukin-1 Receptor Antagonist to Acute Psychosocial Stress." Life Sciences, vol. 78, no. 26, 2006, pp. 3082-9.
Rohleder N, Wolf JM, Herpfer I, et al. No response of plasma substance P, but delayed increase of interleukin-1 receptor antagonist to acute psychosocial stress. Life Sci. 2006;78(26):3082-9.
Rohleder, N., Wolf, J. M., Herpfer, I., Fiebich, B. L., Kirschbaum, C., & Lieb, K. (2006). No response of plasma substance P, but delayed increase of interleukin-1 receptor antagonist to acute psychosocial stress. Life Sciences, 78(26), 3082-9.
Rohleder N, et al. No Response of Plasma Substance P, but Delayed Increase of Interleukin-1 Receptor Antagonist to Acute Psychosocial Stress. Life Sci. 2006 May 22;78(26):3082-9. PubMed PMID: 16414081.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - No response of plasma substance P, but delayed increase of interleukin-1 receptor antagonist to acute psychosocial stress. AU - Rohleder,Nicolas, AU - Wolf,Jutta M, AU - Herpfer,Inga, AU - Fiebich,Bernd L, AU - Kirschbaum,Clemens, AU - Lieb,Klaus, Y1 - 2006/01/18/ PY - 2005/09/20/received PY - 2005/11/18/revised PY - 2005/12/09/accepted PY - 2006/1/18/pubmed PY - 2006/6/15/medline PY - 2006/1/18/entrez SP - 3082 EP - 9 JF - Life sciences JO - Life Sci VL - 78 IS - 26 N2 - Psychosocial stress has been shown to induce inflammatory reactions, followed by the release of immunosuppressive glucocorticoids. This may be mediated by catecholamines or other stress reactive substances such as neuropeptides or cytokines. We here set out to explore the effects of acute psychosocial stress on plasma levels of substance P (SP), a possible mediator of stress-induced inflammatory reactions, and interleukin-1 receptor antagonist (IL-1ra). Twelve healthy male subjects (mean age 27 yrs.) were subjected to the psychosocial stress test "Trier Social Stress Test" (TSST) and a resting control condition. Blood and saliva samples were taken before, as well as 1, 20, 45, and 90 min after TSST or rest, respectively. Salivary cortisol and plasma SP and IL-1ra were measured using immunoassays, salivary alpha-amylase (sAA) was measured by an enzyme kinetic method, and plasma epinephrine (E) and norepinephrine (NE) were measured by HPLC. The TSST induced immediate increases of E, NE, and sAA, and a delayed increase of free cortisol. Plasma IL-1ra showed an even further delayed peak at 90 min after stress. Plasma levels of SP did not respond to stress. No significant associations between changes of stress hormones and IL-1ra or SP were found. We conclude that substance P, epinephrine, and norepinephrine are probably not involved in mediating peripheral inflammation following psychosocial stress, at least with respect to IL-1ra. Further studies have to reveal the mechanisms involved in the stress-induced up regulation of IL-1ra. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/16414081/No_response_of_plasma_substance_P_but_delayed_increase_of_interleukin_1_receptor_antagonist_to_acute_psychosocial_stress_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(05)01257-9 DB - PRIME DP - Unbound Medicine ER -