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Glucocorticoid therapy alters hormonal and cytokine responses to endotoxin in man
Abstract
Previous experimental data have demonstrated that steroid pretreatment regulates endotoxin-elicited cytokine production. The timing of such hypercortisolemia also appears to be a major determinant of both the systemic and the cytokine response to infectious stimuli. Our study was undertaken to further study the in vivo influence of glucocorticoid infusion concurrent with and before endotoxin exposure in man. A total of 23 normal human subjects were given endotoxin (LPS) alone or pretreated with hydrocortisone infusion for 6 h immediately before and concomitant to LPS administration; or rendered hypercortisolemic for a 6-h period waiting 6, 12, or 144 h before LPS administration. LPS administration was followed by significant elevations in temperature (1.9 +/- 0.3 degrees C), pulse (29 +/- 6 bpm), and resting energy expenditure (26.2 +/- 0.4 kcal/kg/day) as well as epinephrine (236 +/- 59 pg/ml), cortisol (296 +/- 29), and C-reactive protein (4.2 +/- .03 mg/dl) as compared with base-line values. Levels of TNF and IL-6 that were not detectable before LPS administration, peaked, respectively, at 90 and 120 min after LPS (155 +/- 4 pg/ml, 12 +/- 1 U/ml). Glucocorticoids when given immediately before and concomitant with LPS significantly attenuated the temperature (0.8 +/- 0.01 degrees C) and pulse rate response (10 +/- 3 bpm) seen after LPS alone as well as suppressing peak levels of epinephrine (78 +/- 14 pg/ml) and C-reactive protein (undetected). TNF remained undetectable in this group although the IL-6 response (14 +/- 1 U/ml) was unchanged. With a 6-h interval between hydrocortisone infusion and LPS challenge, changes in temperature, pulse, resting energy expenditure, and hormone levels were similar to those seen after LPS alone whereas TNF remained undetectable and IL-6 levels were similar to subjects receiving LPS alone. Subjects receiving LPS after 12 or 144 h after hydrocortisone infusion displayed hemodynamic and hormonal responses similar to the LPS alone group, yet mounted significantly greater circulating levels of both IL-6 (117 +/- 14 U/ml, 160 +/- 51 U/ml at 12 and 144 h) and TNF (609 +/- 173, 671 +/- 132 pg/ml at 12 and 144 h) to those observed after LPS alone. We conclude that antecedent periods of hypercortisolemia participate in regulation of the hemodynamic, hormonal, and cytokine responses to endotoxin and that a complex temporal relationship between hypercortisolemia and LPS induced cytokine and systemic responses exists.
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“In humans, plasma levels of TNF-α and IL-6 are higher if cortisol is given 12 hr prior to, but not concurrent with, LPS (Barber et al., 1993).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Barber et al., 1993
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Sapolsky, R. M., Romero, L. M., & Munck, A. U. (2000) · Endocrine Reviews · doi:10.1210/edrv.21.1.0389 · Cited by 7,541
“(136) were obtained with large doses of GCs administered to subjects with normal GCs.”
BackgroundInfluentialAnnane, D. (2002) · JAMA · doi:10.1001/jama.288.7.862 · Cited by 3,075
Effect of Prolonged Methylprednisolone Therapy in Unresolving Acute Respiratory Distress Syndrome
Meduri, G. U., Headley, A. S., Golden, E. B., Carson, S. J., Umberger, R. A., Kelso, T. M., & Tolley, E. A. (1998) · JAMA · doi:10.1001/jama.280.2.159 · Cited by 998
Inflammatory cytokines and cell response in surgery
Lin, E., Calvano, S. E., & Lowry, S. F. (2000) · Surgery · doi:10.1067/msy.2000.101584 · Cited by 576
Self-citationPractice parameters for hemodynamic support of sepsis in adult patients: 2004 update
Hollenberg, S. M., Ahrens, T. S., Annane, D., Astiz, M. E., Chalfin, D. B., Dasta, J. F., Heard, S. O., Martin, C., Napolitano, L. M., Susla, G. M., et al. (2004) · Critical Care Medicine · doi:10.1097/01.ccm.0000139761.05492.d6 · Cited by 511
“In another experiment, hydrocortisone given before or concurrent with an intravenous endotoxin challenge in 23 healthy subjects prevented the decreases in blood pressure and increases in heart rate and circulating epinephrine concentrations (156).”
BackgroundAn inflammatory review of glucocorticoid actions in the CNS
Sorrells, S. F., & Sapolsky, R. M. (2006) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2006.11.006 · Cited by 461
Cavaillon, J. (1994) · Biomedicine & Pharmacotherapy · doi:10.1016/0753-3322(94)90005-1 · Cited by 453
Acute Inflammatory Response to Endotoxin in Mice and Humans
Copeland, S., Warren, H. S., Lowry, S. F., Calvano, S. E., & Remick, D. G. (2005) · Clinical and Vaccine Immunology · doi:10.1128/cdli.12.1.60-67.2005 · Cited by 427
“Similar findings have been reported in numerous studies in humans and mice (1, 2, 5, 17, 18, 24, 26, 31, 34, 35).”
ResultSelf-citationThe Stressed CNS: When Glucocorticoids Aggravate Inflammation
Sorrells, S. F., Caso, J. R., Munhoz, C. D., & Sapolsky, R. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.09.032 · Cited by 425
New Insights into the Biology of the Acute Phase Response
Suffredini, A. F., Fantuzzi, G., Badolato, R., Oppenheim, J. J., & O’Grady, N. P. (1999) · Journal of Clinical Immunology · doi:10.1023/a:1020563913045 · Cited by 397
“However, when a stress dose of steroids is administered as long as 6 days prior to the administration of endotoxin, cytokine responses are enhanced (80).”
BackgroundMechanisms of Glucocorticoid-Induced Insulin Resistance
Geer, E. B., Islam, J., & Buettner, C. (2014) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2013.10.005 · Cited by 392
Annane, D., Sebille, V., & Charpentier, C. (2003) · ACC Current Journal Review · doi:10.1016/s1062-1458(02)00997-2 · Cited by 379
“Women 37 (32) 42 (37) 8 (24) 12 (33) 45 (30) 54 (36)”
Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis
Beishuizen, A., & THIJS, L. G. (2003) · Journal of Endotoxin Research · doi:10.1179/096805103125001298 · Cited by 337
Choileain, N. N. (2006) · Archives of Surgery · doi:10.1001/archsurg.141.11.1132 · Cited by 310
Pro- versus anti-inflammatory cytokines: myth or reality.
Cavaillon, J. (2001) · PubMed · Cited by 301
Hack, C. E., Aarden, L. A., & THUS, L. G. (1997) · Advances in immunology · doi:10.1016/s0065-2776(08)60597-0 · Cited by 286
Extensive expertise in endocrinology: adrenal crisis
Allolio, B. (2015) · European Journal of Endocrinology · doi:10.1530/eje-14-0824 · Cited by 251
DeRijk, R. H., Michelson, D., Karp, B., Petrides, J. S., Galliven, E., Deuster, P., Paciotti, G. F., Gold, P. W., & Sternberg, E. M. (1997) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.82.7.4041 · Cited by 250
Papanicolaou, D. A., Petrides, J. S., Tsigos, C., Bina, S., Kalogeras, K. T., Wilder, R. L., Gold, P. W., Deuster, P. A., & Chrousos, G. P. (1996) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1996.271.3.e601 · Cited by 226
Sympathoadrenal System in Stress
Květňanský, R., Pacák, K., Fukuhara, K., Viskupic, E., Hiremagalur, B., Nankova, B. B., Goldstein, D. S., Sabban, E. L., & Kopin, I. J. (1995) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1995.tb44676.x · Cited by 233
Hahner, S., Ross, R. J., Arlt, W., Bancos, I., Burger-Stritt, S., Torpy, D. J., Husebye, E. S., & Quinkler, M. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00252-7 · Cited by 223
Glucocorticoids and stress: permissive and suppressive actions
MUNCK, A., & NÁRAY‐FEJES‐TÓTH, A. (1994) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1994.tb39221.x · Cited by 209
Biochemistry and cell biology of bacterial endotoxins
Holst, O., Ulmer, A. J., Brade, H., Flad, H., & Rietschel, E. (1996) · FEMS Immunology & Medical Microbiology · doi:10.1111/j.1574-695x.1996.tb00126.x · Cited by 196
Mechanisms of Fever Production and Lysis: Lessons from Experimental LPS Fever
Roth, J., & Blatteis, C. M. (2014) · Comprehensive physiology · doi:10.1002/cphy.c130033 · Cited by 206
“In vivo , IL-10 has been shown to depress the production of TNF-α , IL-1 β , and IL-6 in mice in response to systemic LPS (115, 252).”
InfluentialHow psychological stress via hormones and nerve fibers may exacerbate rheumatoid arthritis
Straub, R. H., Dhabhar, F. S., Bijlsma, J. W. J., & Cutolo, M. (2005) · Arthritis & Rheumatism · doi:10.1002/art.20747 · Cited by 175
Heat stress, cytokines, and the immune response to exercise
Starkie, R. L., Hargreaves, M., Rolland, J. M., & Febbraio, M. A. (2005) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2005.03.005 · Cited by 164
HUMAN ENDOTOXEMIA: A MODEL FOR MECHANISTIC INSIGHT AND THERAPEUTIC TARGETING
Lowry, S. F. (2005) · Shock · doi:10.1097/01.shk.0000191340.23907.a1 · Cited by 156
“Glucocorticoid excess, as produced by hydrocortisone injection (100–200 mg) (50) or 6-h infusion (3 mg/kg/min) (7) before LPS challenge abrogates much of the clinical symptoms (including temperature, heart rate, and increased energy expenditure), as well as proinflammatory cytokine and cytokine antagonist appearance a…”
BackgroundInfluentialSelf-citationThe influence of neuroendocrine pathways on lymphocyte migration
Ottaway, C. A., & Husband, A. J. (1994) · Immunology Today · doi:10.1016/0167-5699(94)90206-2 · Cited by 157
Low-dose hydrocortisone infusion attenuates the systemic inflammatory response syndrome
Briegel, J., Kellermann, W., Forst, H., Haller, M., Bittl, M., Hoffmann, G. E., B�chler, M. W., Uhl, W. H., Peter, K., & Phospholipase A2 Study Group (1994) · Journal of Molecular Medicine · doi:10.1007/bf00180547 · Cited by 151
“with a continuous infusion of hydrocortisone (3 gg kg lmin 1) prior to and during endotoxin challenge [1, 2].”
BackgroundImmunotherapy in sepsis - brake or accelerate?
Steinhagen, F., Schmidt, S. V., Schewe, J., Peukert, K., Klinman, D. M., & Bode, C. (2020) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2020.107476 · Cited by 152
Cortisol Exerts bi-phasic Regulation of Inflammation in Humans
Yeager, M. P., Pioli, P. A., & Guyre, P. M. (2010) · Dose-Response · doi:10.2203/dose-response.10-013.yeager · Cited by 145
“These effects have been shown to persist in humans for up to 6 days (Barber et al. 1993).”
BackgroundLong-Term Alterations in Neuroimmune Responses after Neonatal Exposure to Lipopolysaccharide
Lomax, L. B., Mouihate, A., Ellis, S. L., & Pittman, Q. J. (2004) · Journal of Neuroscience · doi:10.1523/jneurosci.1077-04.2004 · Cited by 142
“Glucocorticoids also block transcription of the mRNA of proinflammatory cytokines (Barber et al., 1993; Chai et al., 1996; Tatro, 2000; Franchimont et al., 2003), making it possible that there is an alteration in the profile of proand anti-inflammatory cytokines that is generated in adults after LPS.”
BackgroundImmune Effects of Corticosteroids in Sepsis
Heming, N., Sivanandamoorthy, S., Meng, P., Bounab, R., & Annane, D. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01736 · Cited by 148
“The expression of the MR is downregulated in human endothelial cells exposed to TNF-α (104).”
BackgroundInfluentialStress as a Risk Factor in the Pathogenesis of Rheumatoid Arthritis
Cutolo, M., & Straub, R. H. (2006) · NeuroImmunoModulation · doi:10.1159/000104855 · Cited by 135
Meduri, G. (1996) · European Respiratory Journal · doi:10.1183/09031936.96.09122650 · Cited by 129
“Furthermore, a short-course GC treatment may negatively affect the host response by significantly enhancing cytokine response to LPS for up to 6 days [219].”
BackgroundGlucocorticoid regulation of the inflammatory response to injury
Yeager, M. P., Guyre, P. M., & Munck, A. U. (2004) · Acta Anaesthesiologica Scandinavica · doi:10.1111/j.1399-6576.2004.00434.x · Cited by 127
“amelioration of clinical symptoms (50) and improved”
Corticosteroids in Sepsis: From Bench to Bedside?
Annane, D., & Cavaillon, J. (2003) · Shock · doi:10.1097/01.shk.0000079423.72656.2f · Cited by 123
“In human volunteers, injection of LPS 12 to 144 h after the end of a cortisol infusion was associated with an enhanced plasma levels of TNF and IL-6 as compared with the absence of cortisol pretreatment (110).”
BackgroundMethodvan der Poll, T., Barber, A. E., Coyle, S. M., & Lowry, S. F. (1996) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.81.10.8855809 · Cited by 129
Self-citationLeon, L. R. (2007) · Progress in brain research · doi:10.1016/s0079-6123(06)62024-4 · Cited by 127
Dominance of T-Helper 2–Type Cytokines After Severe Injury
Mack, V. E. (1996) · Archives of Surgery · doi:10.1001/archsurg.1996.01430240057007 · Cited by 123
Successful Antidepressant Therapy Restores the Disturbed Interplay Between TNF-α System and HPA Axis
Himmerich, H., Binder, E. B., Kunzel, H. E., Schuld, A., Lucae, S., Uhr, M., Pollmächer, T., Holsboer, F., & Ising, M. (2006) · Biological Psychiatry · doi:10.1016/j.biopsych.2006.03.075 · Cited by 122
Detoxifying endotoxin: time, place and person
Munford, R. S. (2005) · Journal of Endotoxin Research · doi:10.1179/096805105x35161 · Cited by 152
Corticosteroids for septic shock
Annane, D. (2001) · Critical Care Medicine · doi:10.1097/00003246-200107001-00036 · Cited by 113
Modeling the influence of circadian rhythms on the acute inflammatory response
Scheff, J. D., Calvano, S. E., Lowry, S. F., & Androulakis, I. P. (2010) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2010.03.026 · Cited by 113
“However, exogenous glucocorticoid administration is known to have a differential effect on cytokines; it stimulates the production of anti-inflammatory cytokines while inhibiting the production of pro-inflammatory cytokines (Barber et al., 1993; Barnes, 1998).”
BackgroundSelf-citationStraub, R. H., Vogl, D., Gross, V., Lang, B., Schölmerich, J., & Andus, T. (1998) · American Journal of Gastroenterology · doi:10.1111/j.1572-0241.1998.00535.x · Cited by 114
“A recent study demonstrates an endotoxin-induced IL-6 increase after prior CS therapy (25), whereas CS administration to cultured cells normally inhibits IL-6 production (26).”
BackgroundNeuroimmune and neuroendocrine abnormalities in depression: two sides of the same coin
Horowitz, M. A., & Zunszain, P. A. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12781 · Cited by 119
Clinical review: corticotherapy in sepsis.
Prigent, H., Maxime, V., & Annane, D. (2003) · Critical Care · doi:10.1186/cc2374 · Cited by 113
“Treatment with hydrocortisone simultaneously with or just before administration of lipopolysaccharide also prevents the occurrence of arterial hypotension and the rise of both heart rate and plasma adrenaline levels [43,44].”
BackgroundDelayed cerebral thrombosis after initial good recovery from pneumococcal meningitis
Schut, E. S., Brouwer, M. C., de Gans, J., Florquin, S., Troost, D., & van de Beek, D. (2009) · Neurology · doi:10.1212/wnl.0b013e3181c55d2e · Cited by 106
Exogenous and endogenous glucocorticoids in rheumatic diseases
Buttgereit, F., Burmester, G., Straub, R. H., Seibel, M. J., & Zhou, H. (2011) · Arthritis & Rheumatism · doi:10.1002/art.30070 · Cited by 105
Prednisolone Dose-Dependently Influences Inflammation and Coagulation during Human Endotoxemia
de Kruif, M. D., Lemaire, L. C. J. M., Giebelen, I. A. J., et al. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.178.3.1845 · Cited by 105
“The first two studies (21, 23) used hydrocortisone at a dose of 3 g/kg/min starting 6 h before LPS injection and continuing up to 6 h after LPS injection; hence, these subjects received the equivalent of 18.”
BackgroundMethodMaternal glucocorticoids increase endotoxin-induced lung inflammation in preterm lambs
Kallapur, S. G., Kramer, B. W. W., Moss, T. J. M., Newnham, J. P., Jobe, A. H., Ikegami, M., & Bachurski, C. J. (2003) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00344.2002 · Cited by 100
“In healthy adult humans, intravenous cortisol infusions given 12 h or 6 days before intravenous Endo increased systemic TNF- , soluble TNF- receptor, and IL-6 levels 2 h after infusion compared with volunteers receiving Endo alone (5, 6).”
MethodHigh prevalence of decreased cortisol reserve in brain-dead potential organ donors
Dimopoulou, I., Tsagarakis, S., Anthi, A., Milou, E., Ilias, Ι., Stavrakaki, K., Charalambidis, C., Tzanela, M., Orfanos, S. E., Mandragos, K. E., et al. (2003) · Critical Care Medicine · doi:10.1097/01.ccm.0000059644.54819.67 · Cited by 95
DeRijk, R. H., Petrides, J. S., Deuster, P. A., Gold, P. W., & Sternberg, E. M. (1996) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.81.1.8550757 · Cited by 100
“LPS is a prototypic stimulus for the release of cytokines from circulating leukocytes that has been extensively validated (3, 4).”
BackgroundHigh-Dose Dexamethasone Accentuates Nuclear Factor- κ B Activation in Endotoxin-Treated Mice
Sadikot, R. T., Jansen, D., Blackwell, T. R., Zoia, O., Yull, F. E., Christman, J. W., & BLACKWELL, T. S. (2001) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.164.5.2008059 · Cited by 94
Neurohormonal Host Defense in Endotoxin Shock
Berczi, I. (1998) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1998.tb09617.x · Cited by 96
Catecholamines increase monocyte TNF receptors and inhibit TNF through β2-adrenoreceptor activation
Guirao, X., Kumar, A., Katz, J. A., Smith, M. G., Lin, E., Keogh, C., Calvano, S. E., & Lowry, S. F. (1997) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1997.273.6.e1203 · Cited by 96
Self-citationStress and aging act through common mechanisms to elicit neuroinflammatory priming
Fonken, L. K., Frank, M. G., Gaudet, A. D., & Maier, S. F. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.07.012 · Cited by 98
“Both the timing (Barber et al., 1993; Frank et al., 2010c) and dose (Dhabhar and McEwen, 1999; Lim et al.”
Diffuse Cerebral Intravascular Coagulation and Cerebral Infarction in Pneumococcal Meningitis
Vergouwen, M. D. I., Schut, E. S., Troost, D., & van de Beek, D. (2010) · Neurocritical Care · doi:10.1007/s12028-010-9387-5 · Cited by 97
“High-dose glucocorticoids can tip the balance toward sustained coagulation and platelet aggregation by influencing the tissue factor/factor VII pathway [20, 21].”
BackgroundGlucocorticoids Increase Excitotoxic Injury and Inflammation in the Hippocampus of Adult Male Rats
Sorrells, S. F., Munhoz, C. D., Manley, N. C., Yen, S., & Sapolsky, R. M. (2014) · Neuroendocrinology · doi:10.1159/000367849 · Cited by 90
Spies, C. M., Strehl, C., van der Goes, M. C., Bijlsma, J. W. J., & Buttgereit, F. (2011) · Best Practice & Research Clinical Rheumatology · doi:10.1016/j.berh.2011.11.002 · Cited by 108
Diurnal Variations in the Human Host Response to Endotoxin
Pollmächer, T., Mullington, J. M., Korth, C., Schreiber, W., Hermann, D. M., Orth, A., Galanos, C., & Holsboer, F. (1996) · The Journal of Infectious Diseases · doi:10.1093/infdis/174.5.1040 · Cited by 90
“Pharmacologic doses of glucocorticoids suppress endotoxin-induced TNF-a release [36-39].”
BackgroundInflammatory Mediators and Intestinal Injury
Caplan, M. S., & MacKendrick, W. (1994) · Clinics in Perinatology · doi:10.1016/s0095-5108(18)30343-9 · Cited by 86
Nicotine exposure altersin vivohuman responses to endotoxin
Wittebole, X., Hahm, S. J., Coyle, S. M., Kumar, A., Calvano, S. E., & Lowry, S. F. (2006) · Clinical & Experimental Immunology · doi:10.1111/j.1365-2249.2006.03248.x · Cited by 86
Self-citationGlucocorticoids in the treatment of severe sepsis and septic shock
Annane, D. (2005) · Current Opinion in Critical Care · doi:10.1097/01.ccx.0000176691.95562.43 · Cited by 85
Meng, X., & Harken, A. H. (2002) · Shock · doi:10.1097/00024382-200205000-00001 · Cited by 81
“Glucocorticoids suppress TNF- gene transcription in human peripheral blood monocytes (58) and they attenuate TNF- production in humans challenged with LPS (59).”
BackgroundA Review of the Adrenal Cortex and Severe Inflammation: Quest of the ???Eucorticoid??? State
Burchard, K. W. (2001) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/00005373-200110000-00033 · Cited by 74
Frankenberger, M., Menzel, M., Betz, R., Kaßner, G., Weber, N., Kohlhäufl, M. J., Häussinger, K., & Ziegler‐Heitbrock, L. (2004) · Clinical & Experimental Immunology · doi:10.1111/j.1365-2249.2004.02637.x · Cited by 78
Immunomodulation in septic shock: hydrocortisone differentially regulates cytokine responses.
Briegel, J., Jochum, M., Gippner‐Steppert, C., & Thiel, M. (2001) · PubMed · Cited by 75
Smyth, G. P., Stapleton, P. P., Freeman, T. A., Concannon, E. M., Mestre, J. R., Duff, M., Maddali, S., & Daly, J. M. (2004) · Journal of Surgical Research · doi:10.1016/s0022-4804(03)00300-7 · Cited by 72
“[22] found that human subjects receiving LPS 12 and 144 h after discontinuation of a cortisol infusion demonstrated significantly higher circulating levels of both IL-6 and TNF- .”
BackgroundSamra, J. S., Summers, L. K. M., & Frayn, K. N. (1996) · British journal of surgery · doi:10.1046/j.1365-2168.1996.02445.x · Cited by 84
The stressful condition as a nutritionally dependent adaptive dichotomy
Ingenbleek, Y., & Bernstein, L. H. (1999) · Nutrition · doi:10.1016/s0899-9007(99)00009-x · Cited by 73
Experimental and Clinical Studies
Sarkar, N. (2005) · Cited by 70
Foteinou, P. T., Calvano, S. E., Lowry, S. F., & Androulakis, I. P. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004706 · Cited by 64
“Thus, in [35] normal human subjects were exposed to glucocorticoid infusion concurrent with and before the endotoxin challenge.”
BackgroundSelf-citationSpielmann, S., Kerner, T., Ahlers, O., Keh, D., Gerlach, M., & Gerlach, H. (2001) · Acta Anaesthesiologica Scandinavica · doi:10.1034/j.1399-6576.2001.045003364.x · Cited by 65
“In addition to possible shedding, direct damage of tissue as well as a disturbed macro- and microcirculation with subsequent ischaemia/reperfusion as well as psychoneurological stimuli (29, 30) are suggested to trigger the activation of TNFa receptors (3).”
BackgroundLauw, F. N., ten Hove, T., Dekkers, P. E. P., de Jonge, E., van Deventer, S. J. H., & van der Poll, T. (2000) · Infection and Immunity · doi:10.1128/iai.68.3.1014-1018.2000 · Cited by 65
“Both cortisol and epinephrine have been reported to inhibit the release of TNF and IL-6 during human endotoxemia (3, 31) while upregulating the release of IL-10 (30, 31).”
BackgroundEffects of antirheumatic agents on cytokines
Barrera, P., Boerbooms, A. M. T., Putte, L. B. A. V. D., et al. (1996) · Seminars in Arthritis and Rheumatism · doi:10.1016/s0049-0172(96)80035-7 · Cited by 65
Mengozzi, M., Fantuzzi, G., Faggioni, R., Marchant, A., Goldman, M., Orencole, S. F., Clark, B. D., Sironi, M., Benigni, F., & Ghezzi, P. (1994) · PubMed Central · Cited by 64
RELATIONSHIP OF BASAL HEART RATE VARIABILITY TO IN VIVO CYTOKINE RESPONSES after endotoxin exposure
Jan, B. U., Coyle, S. M., Macor, M., Reddell, M. T., Calvano, S. E., & Lowry, S. F. (2010) · Shock · doi:10.1097/shk.0b013e3181b66bf4 · Cited by 61
“As previously described, a radial arterial catheter was placed (0700 h) the morning of study day (36, 37).”
MethodSelf-citationSantarsieri, M., Niyonkuru, C., McCullough, E. H., Dobos, J. A., Dixon, C., Berga, S. L., & Wagner, A. K. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3177 · Cited by 60
“77,78 Studies also show that elevated cortisol levels impair synaptic plasticity and cognition, decrease neurogenesis, and cause dendritic atrophy.”
Meduri, G. U. (1999) · Sepsis · doi:10.1023/a:1009870524359 · Cited by 59
Vedder, H., Schreiber, W., Yassouridis, A., Gudewill, S., Galanos, C., & Pollmächer, T. (1999) · Inflammation Research · doi:10.1007/s000110050408 · Cited by 58
“It has been shown by human in vivo [28] and in vitro studies [36] that glucocorticoids are crucially involved in the shut-off of the biosynthesis of TNF-a after stimulation with endotoxin.”
BackgroundResultDexamethasone Enhances ATP-Induced Inflammatory Responses in Endothelial Cells
Ding, Y., Gao, Z., Jacobson, K. A., & Suffredini, A. F. (2010) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.110.171975 · Cited by 63
“The release of stress hormones (e.g., cortisol, catecholamines) during injury or serious infections may alter the subsequent host responses to inflammatory stimuli (Barber et al., 1993; van der Poll et al., 1996).”
BackgroundStress and Autoimmune Thyroid Diseases
Bagnasco, M., Bossert, I., & Pesce, G. (2006) · NeuroImmunoModulation · doi:10.1159/000104859 · Cited by 59
The antiglucocorticoid action of mifepristone
Agarwal, M. K. (1996) · Pharmacology & Therapeutics · doi:10.1016/0163-7258(96)00016-2 · Cited by 58
Glucocorticoids and Inflammation: A Double-Headed Sword in Depression?
Horowitz, M. A., Zunszain, P. A., Anacker, C., Musaelyan, K., & Pariante, C. M. (2013) · Modern Trends in Psychiatry · doi:10.1159/000343980 · Cited by 57
Glucocorticoid Treatment in Acute Lung Injury and Acute Respiratory Distress Syndrome
Marik, P. E., Meduri, G. U., Rocco, P. R. M., & Annane, D. (2011) · Critical Care Clinics · doi:10.1016/j.ccc.2011.05.007 · Cited by 58
Experimental Human Endotoxemia: A Model of the Systemic Inflammatory Response Syndrome?
Calvano, S. E., & Coyle, S. M. (2012) · Surgical Infections · doi:10.1089/sur.2012.155 · Cited by 57
Self-citationCorticosterone exerts immunostimulatory effects on macrophages via endoplasmic reticulum stress
Zhou, J.-Y., Zhong, H.-J., Yang, C., Yan, J., Wang, H.-Y., & Jiang, J.-X. (2010) · British journal of surgery · doi:10.1002/bjs.6820 · Cited by 57
Role of interleukin-10 on hyporesponsiveness of endotoxin during surgery
Ogata, M., Okamoto, K., KOHRIYAMA, K., et al. (2000) · Critical Care Medicine · doi:10.1097/00003246-200009000-00007 · Cited by 57
Endogenous antipyretics: neuropeptides and glucocorticoids
Roth, J. (2004) · Frontiers in bioscience · doi:10.2741/1277 · Cited by 56
“Treatment with GCs is frequently accompanied by reduced fever under experimental or clinical conditions (92, 94, 95).”
BackgroundBARBER, A., Coyle, S., Fischer, E., Smith, C. R., van der Poll, T., Shires, G. T., & LOWRY, S. (1995) · Surgery · doi:10.1016/s0039-6060(05)80352-6 · Cited by 56
Self-citationSepsis, Severe Sepsis, and Septic Shock
Munford, R. S., & Suffredini, A. F. (2010) · Elsevier eBooks · doi:10.1016/b978-0-443-06839-3.00070-9 · Cited by 55
Role of endotoxin and cytokines in the systemic inflammatory response to heat injury
Leon, L. R. (2010) · Frontiers in Bioscience-Scholar · doi:10.2741/s111 · Cited by 54
“Glucocorticoid therapy Glucocorticoid hormones (cortisol in humans, corticosterone in rodents) are an integral component of the hypothalamic-pituitary-adrenal (HPS) axis, whose main actions are mobilization of energy stores and inhibition of cytokine production in response to stress (146-148).”
BackgroundButtgereit, F., Zhou, H., Kalak, R., Gaber, T., Spies, C. M., Huscher, D., Straub, R. H., Modzelewski, J. R. K., Dunstan, C. R., & Seibel, M. J. (2009) · Arthritis & Rheumatism · doi:10.1002/art.24619 · Cited by 54
Alvarez, S. M., Karavidas, M. K., Coyle, S. M., Lu, S., Macor, M., Oikawa, L. O., Lehrer, P. M., Calvano, S. E., & Lowry, S. F. (2007) · Journal of Endotoxin Research · doi:10.1177/0968051907086465 · Cited by 53
Self-citationThe Human Response to Endotoxin
Lin, E., & Lowry, S. F. (1998) · Sepsis · doi:10.1023/a:1009890031293 · Cited by 54
Self-citationGlucocorticoid action and the development of selective glucocorticoid receptor ligands
Cole, T. J. (2006) · Biotechnology annual review · doi:10.1016/s1387-2656(06)12008-6 · Cited by 56
Duration of Glucocorticoid Treatment and Outcome in Sepsis
Meduri, G. U., & Chrousos, G. P. (1998) · CHEST Journal · doi:10.1378/chest.114.2.355-a · Cited by 54
Assis, V. R., Titon, S. C. M., Queiroz‐Hazarbassanov, N., Massoco, C. D. O., & Gomes, F. R. (2017) · Journal of Experimental Zoology Part A Ecological and Integrative Physiology · doi:10.1002/jez.2093 · Cited by 53
Lipopolysaccharide-induced apoptosis in swine lymphocytes in vivo
Norimatsu, M., Ono, T., Aoki, A., Ohishi, K., Takahashi, T., Watanabe, G., Taya, K., Sasamoto, S., & Tamura, Y. (1995) · Infection and Immunity · doi:10.1128/iai.63.3.1122-1126.1995 · Cited by 52
Metadata
- Authors
- Barber, A. E., Coyle, S. M., Marano, M. A., Fischer, E., Calvano, S. E., Fong, Y., Moldawer, L. L., & Lowry, S. F.
- Affiliations
- Cornell University (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1993-03-01
- Volume
- 150
- Issue
- 5
- Pages
- 1999-2006
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1514001940
- Cited by
- 285
- References
- 0
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 6 · 2015: 4 · 2014: 13 · 2013: 9 · 2012: 5
- FWCI
- 11.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca052108-02)
- National Cancer Institute (CA-52108)
- National Institute of General Medical Sciences (GM40586, GM-34695)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- glucocorticoid pretreatment, cortisol, endotoxin, lipopolysaccharide, cytokine response, TNF-α, interleukin-6, C-reactive protein, hypercortisolism, fever, epinephrine, resting energy expenditure, timing of steroid administration, endotoxemia, research participants
- MeSH terms
- Adult, Body Temperature, Endotoxins, Epinephrine, Glucocorticoids, Humans, Hydrocortisone, Interferon-gamma, Lipopolysaccharides, Norepinephrine, Tumor Necrosis Factor-alpha, Interleukin-6
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