Modulation of miR-155 and miR-125b Levels following Lipopolysaccharide/TNF-{alpha} Stimulation and Their Possible Roles in Regulating the Response to Endotoxin Shock
Tili et al.
J. Immunol. 2007;179:5082-5089.
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Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women
Motton et al.
Am. J. Clin. Nutr. 2007;85:60-65.
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Tumor Necrosis Factor-{alpha} Induces Skeletal Muscle Insulin Resistance in Healthy Human Subjects via Inhibition of Akt Substrate 160 Phosphorylation
Plomgaard et al.
Diabetes 2005;54:2939-2945.
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Coagulation Factor Xa Stimulates Interleukin-8 Release in Endothelial Cells and Mononuclear Leukocytes: Implications in Acute Myocardial Infarction
Busch et al.
Arterioscler. Thromb. Vasc. Bio. 2005;25:461-466.
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Effect of interleukin-1beta and tumor necrosis factor-alpha on gene expression in human endothelial cells
Zhao et al.
Am. J. Physiol. Cell Physiol. 2003;284:C1577-C1583.
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Syndecan-4 Deficiency Leads to High Mortality of Lipopolysaccharide-injected Mice
Ishiguro et al.
J. Biol. Chem. 2001;276:47483-47488.
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GH Strongly Affects Serum Concentrations of Mannan-Binding Lectin: Evidence for a New IGF-I Independent Immunomodulatory Effect of GH
Hansen et al.
J. Clin. Endocrinol. Metab. 2001;86:5383-5388.
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Azathioprine hypersensitivity
SOFAT et al.
Ann Rheum Dis 2001;60:719a-721.
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Role of p38 mitogen-activated protein kinase in cardiac myocyte secretion of the inflammatory cytokine TNF-{alpha}
Ballard-Croft et al.
Am. J. Physiol. Heart Circ. Physiol. 2001;280:H1970-H1981.
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Inflammatory Cytokines in Nonpathological States
Cannon
Physiology 2000;15:298-303.
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Prolonged survival of mice with Pseudomonas aeruginosa-induced sepsis by rIL-12 modulation of IL-10 and interferon-{gamma}
YAMAGUCHI et al.
J Med Microbiol 2000;49:701-707.
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Adverse Ventilatory Strategy Causes Pulmonary-to-Systemic Translocation of Endotoxin
MURPHY et al.
Am. J. Respir. Crit. Care Med. 2000;162:27-33.
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Drew-Anderson technique attenuates systemic inflammatory response syndrome and improves respiratory function after coronary artery bypass grafting
Richter et al.
Ann. Thorac. Surg. 2000;69:77-83.
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Salmonella typhi Flagella Are Potent Inducers of Proinflammatory Cytokine Secretion by Human Monocytes
Wyant et al.
Infect. Immun. 1999;67:3619-3624.
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The Role of p38 Mitogen-Activated Protein Kinase in IL-1{beta} Transcription
Baldassare et al.
J. Immunol. 1999;162:5367-5373.
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LPS Challenge in D-galactosamine-Sensitized Mice Accounts for Caspase-dependent Fulminant Hepatitis, not for Septic Shock
MIGNON et al.
Am. J. Respir. Crit. Care Med. 1999;159:1308-1315.
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IL-18-deficient mice are resistant to endotoxin-induced liver injury but highly susceptible to endotoxin shock
Sakao et al.
Int Immunol 1999;11:471-480.
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Modulation of Mouse Endotoxin Shock by Inhibition of Phosphatidylcholine-Specific Phospholipase C
Tschaikowsky et al.
J. Pharmacol. Exp. Ther. 1998;285:800-804.
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Tumor necrosis factor in the heart
Meldrum
Am. J. Physiol. Regul. Integr. Comp. Physiol. 1998;274:R577-R595.
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Transplantation Immunology
VanBuskirk et al.
JAMA 1997;278:1993-1999.
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Immunopharmacology: Immunomodulation and Immunotherapy
Ballow and Nelson
JAMA 1997;278:2008-2017.
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Notoginsenoside R1 Counteracts Endotoxin-Induced Activation of Endothelial Cells In Vitro and Endotoxin-Induced Lethality in Mice In Vivo
Zhang et al.
Arterioscler. Thromb. Vasc. Bio. 1997;17:465-474.
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Prevention of Jarisch-Herxheimer Reactions by Treatment with Antibodies against Tumor Necrosis Factor {alpha}
Fekade et al.
NEJM 1996;335:311-315.
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N-Acetylcysteine Inhibits Production of Tumor Necrosis Factor a and Interleukin-1{beta}
Redondo and Subira
Arch Intern Med 1996;156:1238-1241.
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The protein kinase C activator PMA modulates LPS lethality in normal mice and protects against LPS lethality in D-galactosamine-sensitized mice
Silverstein et al.
Innate Immunity 1996;3:29-37.
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Pathogenesis and Treatment of the Adult Respiratory Distress Syndrome
Fulkerson et al.
Arch Intern Med 1996;156:29-38.
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Interleukin-13 Effectively Down-regulates the Monocyte Inflammatory Potential During Traumatic Stress
Kim et al.
Arch Surg 1995;130:1330-1336.
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Acute Pancreatitis Induces Intrapancreatic Tumor Necrosis Factor Gene Expression
Norman et al.
Arch Surg 1995;130:966-970.
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Editorial
Morrison
Innate Immunity 1995;2:149-150.
Effects of bactericidal/permeability-increasing protein on endotoxin-induced fever and Escherichia coli-induced shock in rabbits
Porat et al.
Innate Immunity 1995;2:9-18.
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Recombinant Human Interleukin 1 Receptor Antagonist in the Treatment of Patients With Sepsis Syndrome: Results From a Randomized, Double-blind, Placebo-Controlled Trial
Fisher et al.
JAMA 1994;271:1836-1843.
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Projected Impact of Monoclonal Anti-Endotoxin Antibody Therapy
Bates and Lee
Arch Intern Med 1994;154:1241-1249.
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Bacterial endotoxins and pathogenesis of Gram-negative infections: current status and future direction
Morrison et al.
Innate Immunity 1994;1:71-83.
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Case 12-1994- A 72-Year-Old Man with Chronic Leg Ulceration and Progressive Renal Failure
Harrington and Colvin
NEJM 1994;330:847-854.
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The Clinical Evaluation of New Drugs for Sepsis: A Prospective Study Design Based on Survival Analysis
Knaus et al.
JAMA 1993;270:1233-1241.
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and interleukin 8, are discussed. Laboratory investigations suggest that these cytokines play a critical role in SIRS by promoting the biochemical and clinical characteristics of SIRS. The biochemical changes induced by TNF and IL-1 include increased synthesis of nitric oxide, prostaglandins, platelet-activating factor, and endothelial cell adhesion molecules. Specific blockade of TNF using neutralizing antibodies or soluble receptors to TNF in animal models of SIRS reduces mortality and severity of disease. Similar results have been observed blocking IL-1 using soluble IL-1 receptors or IL-1 receptor antagonists. Preliminary clinical studies suggest that blockade may be useful in treating human SIRS. The various strategies for blocking IL-1 and TNF are presented; in addition, their mechanism(s) of action and safety in humans are discussed. We conclude that based on animal studies and preliminary clinical trials, strategies to block IL-1 or TNF may benefit patients with the syndrome, although thorough clinical trials have not been completed.