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Increased susceptibility to disseminated Candidiasis in interleukin-6 deficient mice.
van Enckevoort F, Netea MG, Hermus A, Sweep CG, van der Meer JW, Kullberg BJ; Interscience Conference on Antimicrobial Agents and Chemotherapy. Abstr Intersci Conf Antimicrob Agents Chemother Intersci Conf Antimicrob Agents Chemother. 1998 Sep 24-27; 38: 296 (abstract no. G-43).
Univ. Hosp. Nijmegen, The Netherlands.
Interleukin-6 (IL-6) is a multifunctional cytokine that regulates multiple aspects of the innate immune response. It has been recently shown that endogenous IL-6 is crucial for an efficient defense against severe infections with Gram- negative and Gram-positive bacteria. The aim of the present study was to investigate the role of endogenous IL-6 in the defense against infection with the yeast Candida albicans. When infected with 3x10(5) CFU/mouse, IL-6 deficient mice (IL-6-/-) had a significantly decreased survival when compared with IL-6+/+ controls (30 vs. 70%, p<0.05). href="http://gateway.nlm.nih.gov/MeetingAbstracts/102188063.html">http://gateway.nlm.nih.gov/MeetingAbstracts/102188063.html
Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats
Auteur(s) / Author(s)ANDO T. (1) ; RIVIER J. (2) ; YANAIHARA H. (1) ; ARIMURA A. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)(1) United States-Japan Biomedical Research Laboratories, Tulane University Hebert Center, Belle Chasse, Louisiana 70037-3001, ETATS-UNIS(2) Peptide Biology Laboratory, Salk Institute, La Jolla, California 92037, ETATS-UNIS
Résumé / AbstractWe 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,CαMeLeu37]-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.
http://cat.inist.fr/?aModele=afficheN&cpsidt=1770729
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Effects of Sleep and Sleep Deprivation on Interleukin-6, Growth Hormone, Cortisol, and Melatonin Levels in Humans1
ReplyDeleteLaura Redwine, Richard L. Hauger, J. Christian Gillin and Michael Irwin
Department of Psychiatry, University of California and San Diego Veterans Healthcare System, San Diego, California 92161
Address all correspondence and requests for reprints to: Michael Irwin, M.D., Department of Psychiatry V116A, San Diego Veterans Affairs Healthcare System, 3350 La Jolla Village Drive, San Diego, California 92161. E-mail: mirwin@ucsd.edu.
The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography.
Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1–2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep.
Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.
http://jcem.endojournals.org/cgi/content/abstract/85/10/3597
http://jcem.endojournals.org/cgi/content/abstract/85/10/3597
ReplyDeleteEffects of Sleep and Sleep Deprivation on Interleukin-6, Growth Hormone, Cortisol, and Melatonin Levels in Humans1
Laura Redwine, Richard L. Hauger, J. Christian Gillin and Michael Irwin
Department of Psychiatry, University of California and San Diego Veterans Healthcare System, San Diego, California 92161
Address all correspondence and requests for reprints to: Michael Irwin, M.D., Department of Psychiatry V116A, San Diego Veterans Affairs Healthcare System, 3350 La Jolla Village Drive, San Diego, California 92161. E-mail: mirwin@ucsd.edu.
The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography.
Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1–2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep.
Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.
Partial night sleep deprivation reduces natural killer and cellular immune responses in humans
ReplyDeleteM Irwin, J McClintick, C Costlow, M Fortner, J White and JC Gillin
Department of Psychiatry, University of California, San Diego, USA.
Prolonged and severe sleep deprivation is associated with alterations of natural and cellular immune function. To determine whether alterations of immune function also occur after even a modest loss of sleep, the effects of early-night partial sleep deprivation on circulating numbers of white blood cells, natural killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleukin-2 (IL-2) production were studied in 42 medically and psychiatrically healthy male volunteers. After a night of sleep deprivation between 10 P.M. and 3 A.M., a reduction of natural immune responses as measured by NK cell activity, NK activity per number of NK cells, LAK activity, and LAK activity per number of LAK precursors (CD16,56, CD25) was found. In addition, concanavalin A-stimulated IL-2 production was suppressed after sleep deprivation due to changes in both adherent and nonadherent cell populations. After a night of recovery sleep, NK activity returned to baseline levels and IL-2 production remained suppressed. These data implicate sleep in the modulation of immunity and demonstrate that even a modest disturbance of sleep produces a reduction of natural immune responses and T cell cytokine production.
http://www.fasebj.org/cgi/content/abstract/10/5/643