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Am J Physiol Regul Integr Comp Physiol 275: R1461-R1467, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 5, R1461-R1467, November 1998

Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats

Tetsuya Ando1, Jean Rivier2, Hitoshi Yanaihara1, and Akira Arimura1

1 United States-Japan Biomedical Research Laboratories, Tulane University Hebert Center, Belle Chasse, Louisiana 70037-3001; and 2 Peptide Biology Laboratory, Salk Institute, La Jolla, California 92037

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [D-Phe12,Nle21,38,Calpha MeLeu37]-anti-human rat (h/r) CRF12-41 (1.5 mg/kg) or cyclo(30---33)[D-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12-41 (Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 µg/kg) or rat urocortin (10 and 100 µg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 µg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.

neuroimmunomodulation; Astressin; [D-Phe12,Nle21,38,Calpha MeLeu37]-anti-human rat corticotropin-releasing factor12-41; urocortin; cytokine


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