Cited by 2,448Sepsis Diagnosis and TreatmentInflammation biomarkers and pathwaysImmune Response and Inflammation

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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

Tracey, Kevin J., Fong, Yuman, Hesse, David G., Manogue, Kirk R., Lee, Annette T., Kuo, George C., Lowry, Stephen F., Cerami, Anthony·1987·Nature

DOI 10.1038/330662a0

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Abstract

Bacterial infection of the mammalian bloodstream can lead to overwhelming sepsis, a potentially fatal syndrome of irreversible cardiovascular collapse (shock) and critical organ failure. Cachectin, also known as tumour necrosis factor, is a macrophage-derived peptide hormone released in response to bacterial lipopolysaccharide, and it has been implicated as a principal mediator of endotoxic shock, although its function in bacterial sepsis is not known. Anaesthetized baboons were passively immunized against endogenous cachectin and subsequently infused with an LD100 dose of live Escherichia coli. Control animals (not immunized against cachectin) developed hypotension followed by lethal renal and pulmonary failure. Neutralizing monoclonal anti-cachectin antibody fragments (F(ab')2) administered to baboons only one hour before bacterial challenge protected against shock, but did not prevent critical organ failure. Complete protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion. These results indicate that cachectin is a mediator of fatal bacteraemic shock, and suggest that antibodies against cachectin offer a potential therapy of life-threatening infection.

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1. Kreger, B. E. W., Craven, D. E. & McCabe, W. R. Am. J. Med. 68, 344-355 (1980). 2. Ziegler, E. J. el al New Engl. J. Med, 307, 1225-1230 (1982). 3. Gilbert, R. P. Physiol. Rev. 40, 245-279 (1960). 4. Beutler, B. & Cerami, A. Nature 320, 584-588 (1986). 5. Beutler, B. & Cerami, A. New Engl. J. Med
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Hsueh, W., Caplan, M. S., Tan, X., MacKendrick, W., & González-Crussí, F. (1998) · Pediatric and Developmental Pathology · doi:10.1007/s100249900002 · Cited by 53
“LPS induces endogenous TNF production [36,41,42] and administration of TNF causes shock [43,44], whereas pretreatment of the animal with anti-TNF [44] ameliorates endotoxin shock and increases survival.”
Lipopolysaccharides induced increases in Fas ligand expression by Kupffer cells via mechanisms dependent on reactive oxygen species
Uchikura, K., Wada, T., Hoshino, S., Nagakawa, Y., Aiko, T., Bulkley, G. B., Klein, A. S., & Sun, Z. (2004) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00314.2003 · Cited by 54
Cytokine mRNA expression in whole blood samples from dogs with natural canine distemper virus infection
Gröne, A., Frisk, A.-L., & Baumgärtner, W. (1998) · Veterinary Immunology and Immunopathology · doi:10.1016/s0165-2427(98)00170-6 · Cited by 54
Beneficial effects of interleukin-6 in neonatal mouse models of group B streptococcal disease
Mancuso, G., Tomasello, F., Migliardo, M., Delfino, D., Cochran, J., Cook, J., & Teti, G. (1994) · Infection and Immunity · doi:10.1128/iai.62.11.4997-5002.1994 · Cited by 63
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Background
IGF-I/IGFBP-3 Equilibrates Ratios of Pro- to Anti-inflammatory Cytokines, Which Are Predictors for Organ Function in Severely Burned Pediatric Patients
Jeschke, M. G., Barrow, R. E., Suzuki, F., Rai, J., Benjamin, D., & Herndon, D. N. (2002) · Molecular Medicine · doi:10.1007/bf03402149 · Cited by 54
“sults in vitro and in animal models by increasing survival rates in the state of septicemia ( 2 ,24,25).”
Background
Tumor Necrosis Factor Mediates Impaired Wound Healing in Chronic Abdominal Sepsis
Cooney, R. N., Iocono, J. A., Maish, G. O., Smith, J. S., & Ehrlich, P. (1997) · doi:10.1097/00005373-199703000-00008 · Cited by 54
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Yu, C., Chang, K., Chiu, C.-J., et al. (1989) · Scandinavian Journal of Rheumatology · doi:10.3109/03009748909099924 · Cited by 54
Passive immunization of mice against D factor blocks lethality and cytokine release during endotoxemia.
Block, M. I., van den Berg, M. J. W., McNamara, M. J., Norton, J. A., Fraker, D. L., & Alexander, H. R. (1993) · The Journal of Experimental Medicine · doi:10.1084/jem.178.3.1085 · Cited by 53
“production of other mediators (IL-1 and IL-6) (33-35).”
Background
The pathophysiology of advanced heart failure
Baig, M. K., Mahon, N., McKenna, W. J., Caforio, A. L. P., Bonow, R. O., Francis, G. S., & Gheorghiade, M. (1999) · Heart & Lung · doi:10.1053/hl.1999.v28.a97762 · Cited by 63
17(R)-Resolvin D1 differentially regulates TLR4-mediated responses of primary human macrophages to purified LPS and liveE. coli
Palmer, C. D., Mancuso, C. J., Weiss, J. P., Serhan, C. N., Guinan, E. C., & Levy, O. (2011) · Journal of Leukocyte Biology · doi:10.1189/jlb.0311145 · Cited by 56
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Background
Mannose-Binding Lectin Contributes to Deleterious Inflammatory Response in Pandemic H1N1 and Avian H9N2 Infection
Ling, M. T., Tu, W., Han, Y., Mao, H., Chong, W. P., Guan, J. Z., Liu, M., Lam, K. T., Law, H., Peiris, M. J. S., et al. (2011) · The Journal of Infectious Diseases · doi:10.1093/infdis/jir691 · Cited by 53
“Excessive production of TNF-a causes tissue injury, hemorrhagic shock, and death in mice [39, 40].”
Background
San-Huang-Xie-Xin-Tang attenuates inflammatory responses in lipopolysaccharide-exposed rat lungs
Lo, Y., Lin, Y., Yu, K., et al. (2005) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2005.03.015 · Cited by 53
BMS-182123, a Fungal Metabolite that Inhibits the Production of TNF-.ALPHA. by Macrophages and Monocytes.
Warr, G. A., Veitch, J. A., Walsh, A. W., et al. (1996) · The Journal of Antibiotics · doi:10.7164/antibiotics.49.234 · Cited by 53
Platelet‐activating factor, tumor necrosis factor, hypoxia and necrotizing enterocolitis
Hsueh, W., Caplan, M., Sun, X., Tan, X., MacKendrick, W., & González-Crussí, F. (1994) · Acta Paediatrica · doi:10.1111/j.1651-2227.1994.tb13234.x · Cited by 52
Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression
Kadokami, T., McTiernan, C. F., Kubota, T., Frye, C. S., Bounoutas, G. S., Robbins, P. D., Watkins, S. C., & Feldman, A. M. (2001) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.2001.280.5.h2281 · Cited by 52
“Elevated plasma levels of TNF-a have been reported in a variety of cardiovascular diseases, including acute myocarditis (35), cardiac allograft rejection (8), myocardial infarction (36), and congestive heart failure (32, 34), as well as in endotoxemia (17, 51, 54).”
Background
Tyrphostin AG 556 improves survival and reduces multiorgan failure in canine Escherichia coli peritonitis.
Sevransky, J., Shaked, G., Novogrodsky, A., et al. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119364 · Cited by 53
“Furthermore, therapies directed against endotoxin (10), TNFa (8), and IL-1 b”
BackgroundInfluential
Different Role of Cytokine Mediators in Septic Shock Related to Meningococcal Disease and Surgery/Polytrauma
Waage, A., & Aasen, A. O. (1992) · Immunological Reviews · doi:10.1111/j.1600-065x.1992.tb01416.x · Cited by 52
Interleukin-1
Dinarello, C. A. (1994) · Advances in pharmacology · doi:10.1016/s1054-3589(08)60429-9 · Cited by 53
Inhibition of PI3Kδ Reduces Kidney Infiltration by Macrophages and Ameliorates Systemic Lupus in the Mouse
Suárez‐Fueyo, A., Rojas, J. M., Cariaga-Martínez, A. E., et al. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1400350 · Cited by 52
HMGB1 in the Immunology of Sepsis (Not Septic Shock) and Arthritis
Czura, C. J., Yang, H., Amella, C. A., & Tracey, K. J. (2004) · Advances in immunology · doi:10.1016/s0065-2776(04)84005-7 · Cited by 52
Self-citation
Non-haemorrhagic obstetric shock
Thomson, A. J., & Greer, I. A. (2000) · Best Practice & Research Clinical Obstetrics & Gynaecology · doi:10.1053/beog.1999.0061 · Cited by 52
Alcohol, Tumor Necrosis Factor, and Tuberculosis
Nelson, S., Mason, C. M., Bagby, G. J., & Summer, W. R. (1995) · Alcoholism Clinical and Experimental Research · doi:10.1111/j.1530-0277.1995.tb01467.x · Cited by 52
Pirfenidone Blocks the In Vitro and In Vivo Effects of Staphylococcal Enterotoxin B
Hale, M. L., Margolin, S. B., Krakauer, T., et al. (2002) · Infection and Immunity · doi:10.1128/iai.70.6.2989-2994.2002 · Cited by 52
“Previous investigations have shown that antibodies recognizing TNF- decrease symptoms associated with toxic shock (30, 43).”
Background
Gram-Negative Bacterial Sepsis and Sepsis Syndrome
Dunn, D. L. (1994) · Surgical Clinics of North America · doi:10.1016/s0039-6109(16)46333-4 · Cited by 52
Immunological and physiological responses to aortic surgery: Effect of reperfusion on neutrophil and monocyte activation and pulmonary function
Barry, M. C., Kelly, C. J., Burke, P., Sheehan, S., Redmond, H. P., & Bouchier‐Hayes, D. (1997) · British journal of surgery · doi:10.1002/bjs.1800840422 · Cited by 50
Effect of antitumour necrosis factor treatment on circulating tumour necrosis factor levels and mortality after surgery in jaundiced mice
Bemelmans, M. H. A., Gouma, D. J., Greve, J. W. M., et al. (1993) · British journal of surgery · doi:10.1002/bjs.1800800845 · Cited by 52
Cytokine mediators of septic infections in the normal and granulocytopenic host
Waage, A., & Steinshamn, S. (1993) · European Journal Of Haematology · doi:10.1111/j.1600-0609.1993.tb00156.x · Cited by 52
The effects of recombinant interleukin-1 and recombinant tumor necrosis factor on non-specific resistance to infection
van der Meer, J. W. M. (1989) · Biotherapy · doi:10.1007/bf02170132 · Cited by 52
“IL-1 contribute to death from infection [25, 31, 32 ].”
Background
TNFR1-induced lethal inflammation is mediated by goblet and Paneth cell dysfunction
Hauwermeiren, F. V., Vandenbroucke, R. E., Grine, L., Lodens, S., Wonterghem, E. V., Rycke, R. M. D., Geest, N. D., Hassan, B. A., & Libert, C. (2014) · Mucosal Immunology · doi:10.1038/mi.2014.112 · Cited by 52
Simultaneous onset of acute inflammatory response, sepsis‐like symptoms and intestinal mucosal injury after cancer chemotherapy
Tsuji, E., Hiki, N., Nomura, S., et al. (2003) · International Journal of Cancer · doi:10.1002/ijc.11196 · Cited by 51
Antibiotic‐Induced Endotoxin Release from Bacteria and Its Clinical Significance
Kirikae, T., Nakano, M., & Morrison, D. C. (1997) · Microbiology and Immunology · doi:10.1111/j.1348-0421.1997.tb01203.x · Cited by 52
Effects of tumour necrosis factor‐α on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function
Edmunds, N. J., Lal, H., & Woodward, B. D. (1999) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0702294 · Cited by 51
Lipoteichoic Acid-Induced Nitric Oxide Production Depends on the Activation of Platelet-Activating Factor Receptor and Jak2
Han, S. H., Kim, J. H., Seo, H. S., Martin, M. H., Chung, G., Michalek, S. M., & Nahm, M. H. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.176.1.573 · Cited by 51
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Background
Increased expression of the interleukin 1 receptor on blood neutrophils of humans with the sepsis syndrome.
Fasano, M. B., Cousart, S. L., Neal, S., et al. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115454 · Cited by 51
Tumor necrosis factor-α in macrophages of heart, liver, kidney, and in the pituitary gland
Arras, M., Höche, A., Bohle, R. M., Eckert, P., Riedel, W., & Schaper, J. (1996) · Cell and Tissue Research · doi:10.1007/s004410050618 · Cited by 51
“This has been confirmed by Tracey et al. (1987) and Mathison et al. (1988).”
Background
Tumor necrosis factor alpha promotes replication and pathogenicity of rat cytomegalovirus
Haagmans, B. L., Stals, F. S., van der Meide, P. H., Bruggeman, C. A., Horzinek, M. C., & Schijns, V. E. C. J. (1994) · Journal of Virology · doi:10.1128/jvi.68.4.2297-2304.1994 · Cited by 51
Sepsis, Signals, and Surgical Sequelae (A Hypothesis)
MICHIE, H. R. (1990) · Archives of Surgery · doi:10.1001/archsurg.1990.01410160119023 · Cited by 51
Endotoxin induction of tumor necrosis factor is enhanced by acid-labile interferon-alpha in acquired immunodeficiency syndrome.
Lau, A. S. Y., & Livesey, J. F. (1989) · Journal of Clinical Investigation · doi:10.1172/jci114231 · Cited by 51
Inhibition of tumor necrosis factor-α (TNF-α)/ TNF-α receptor binding by structural analogues of suramin§§Abbreviations: TNF-α, tumor necrosis factor-α; and MC/EM, MonteCarlo/energy minimization.
Mancini, F., Toro, C. M., Mabilia, M., Giannangeli, M., Pinza, M., & Milanese, C. (1999) · Biochemical Pharmacology · doi:10.1016/s0006-2952(99)00150-1 · Cited by 50
Maternal Death Following Cardiopulmonary Collapse After Delivery: Amniotic Fluid Embolism or Septic Shock Due to Intrauterine Infection?
Romero, R. J., Kadar, N. R., Vaisbuch, E., & Hassan, S. S. (2010) · American Journal of Reproductive Immunology · doi:10.1111/j.1600-0897.2010.00823.x · Cited by 48
Protective Effects of Polydatin on Septic Lung Injury in Mice via Upregulation of HO-1
Li, X., Gong, X., Zhang, L., et al. (2013) · Mediators of Inflammation · doi:10.1155/2013/354087 · Cited by 50
Mast Cell Stabilization Improves Survival by Preventing Apoptosis in Sepsis
Ramos, L., Peña, G., Cai, B., Deitch, E. A., & Ulloa, L. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1000273 · Cited by 51
“A classical example is that anti-TNF therapies can prevent sepsis in the early stages when the treatment is started before the challenge (41), but these approaches failed in clinical trials, because they are ineffectivewhen administered after the septic challenge (4, 42, 43).”
Background
GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia
Granado, M., Martı́n, A. I., López-Menduiña, M., et al. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00308.2007 · Cited by 50
Advances in Sepsis Therapy
Gl�ck, T., & Opal, S. M. (2004) · Drugs · doi:10.2165/00003495-200464080-00004 · Cited by 50
TNF-α and myocardial depression in endotoxemic rats: temporal discordance of an obligatory relationship
Meng, X., Ao, L., Meldrum, D. R., Cain, B. S., Shames, B. D., Selzman, C. H., Banerjee, A. M., & Harken, A. H. (1998) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1998.275.2.r502 · Cited by 50
The physiology of nutritional assessment and therapy in protein-calorie malnutrition.
McMahon, M., & Bristrian, B. R. (1990) · Disease-a-month : DM · doi:10.1016/0011-5029(90)90018-m · Cited by 45
Free radicals and septic shock in primates: The role of tumor necrosis factor
Lloyd, S. S., Chang, A. K., Taylor, F. B., Janzen, E. G., & McCay, P. B. (1993) · Free Radical Biology and Medicine · doi:10.1016/0891-5849(93)90020-u · Cited by 49
New strategies for combatting sepsis: the magic bullets missed the mark…but the search continues
Quezado, Z., Banks, S. M., & Natanson, C. (1995) · Trends in biotechnology · doi:10.1016/s0167-7799(00)88906-4 · Cited by 50
Anti-Tumor Necrosis Factor Antibodies Inhibit the Influx of Granulocytes and Monocytes into an Inflammatory Exudate and Enhance the Growth of Listeria monocytogenes in Various Organs
van Furth, R., van Zwet, T. L., Buisman, A., et al. (1994) · The Journal of Infectious Diseases · doi:10.1093/infdis/170.1.234 · Cited by 50
Monoclonal Antibody to Endotoxin Core Protects Mice from Escherichia coli Sepsis by a Mechanism Independent of Tumor Necrosis Factor and Interleukin-6
Silva, A. T., Appelmelk, B. J., Buurman, W. A., Bayston, K. F., & Cohen, J. (1990) · The Journal of Infectious Diseases · doi:10.1093/infdis/162.2.454 · Cited by 49
“It has been shown that antibody to TNF protects mice from endotoxin-induced injury [10] and baboons from Escherichia coli sepsis [11].”
Background
Control of Fecal Peritoneal Infection in Mice by Colony-Stimulating Factors
Barsig, J., Bundschuh, D. S., Härtung, T., et al. (1996) · The Journal of Infectious Diseases · doi:10.1093/infdis/174.4.790 · Cited by 50
ABSENCE OF ENDOGENOUS INTERLEUKIN-6 ENHANCES THE INFLAMMATORY RESPONSE DURING ACUTE PANCREATITIS INDUCED BY CERULEIN IN MICE
Cuzzocrea, S., Mazzon, E., Dugo, L., et al. (2002) · Cytokine · doi:10.1006/cyto.2002.0883 · Cited by 49
Soluble, but Not Transmembrane, TNF-α Is Required during Influenza Infection To Limit the Magnitude of Immune Responses and the Extent of Immunopathology
DeBerge, M., Ely, K. H., & Enelow, R. I. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1302729 · Cited by 48
Matrix metalloproteinases contribute to endotoxin and interleukin‐1β induced vascular dysfunction
Lalu, M. M., Cena, J., Chowdhury, R., Lam, A. P., & Schulz, R. (2006) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0706823 · Cited by 49
“…sepsis and endotoxaemia the initial inflammatory response due to LPS is largely mediated by proinflammatory cytokines (including interleukin-1b (IL-1b) (Hesse et al., 1988) and tumor necrosis factor-a (Tracey et al., 1986, 1987)) which increase the production of a number of downstream effectors.”
Background
Cytokine and chemokine receptor profile of peripheral blood mononuclear cells during treatment with infliximab in patients with active rheumatoid arthritis
Nissinen, R., Leirisalo-Repo, M., Peltomaa, R., Palosuo, T., & Vaarala, O. (2004) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2003.008599 · Cited by 50
TNF-α disruption of lung endothelial integrity: reduced integrin mediated adhesion to fibronectin
Rotundo, R. F., Curtis, T. M., Shah, M. D., Gao, B., Mastrangelo, A. M., LaFlamme, S. E., & Saba, T. M. (2002) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00145.2000 · Cited by 49
“Tumor necrosis factor- (TNF- ), an inflammatory cytokine released from endotoxin-activated monocytes and macrophages sequestered in the lung microcirculation and interstitium during sepsis or lung inflammation, is believed to contribute to disruption of the lung vascular barrier leading to the increase in protein perm…”
Background
Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.
Bernard, C., Szekely, B., Philip, I., Wollman, E. E., Payen, D. M., & Tedgui, A. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115664 · Cited by 48
The effects of pentoxifylline on lipopolysaccharide (LPS) fever, plasma interleukin 6 (IL 6), and tumor necrosis factor (TNF) in the rat
LeMay, L. G., Vander, A. J., & Kluger, M. J. (1990) · Cytokine · doi:10.1016/1043-4666(90)90032-o · Cited by 49
Induction of tumor necrosis factor alpha by the group- and type-specific polysaccharides from type III group B streptococci
Mancuso, G., Tomasello, F. F., von Hunolstein, C., et al. (1994) · Infection and Immunity · doi:10.1128/iai.62.7.2748-2753.1994 · Cited by 49
“These effects are clearly observed in sepsis models involving intravascular injection of endotoxin (5) or whole gram-positive (10) and gramnegative (10, 29, 36) bacteria.”
Background
Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis
Chikanza, I. C., Roux-Lombard, P., DAYER, J.-M., & Panayi, G. S. (1993) · Clinical & Experimental Immunology · doi:10.1111/j.1365-2249.1993.tb05941.x · Cited by 47
Recombinant bovine somatotropin blunts plasma tumor necrosis factor-alpha, cortisol, and thromboxane-B2 responses to endotoxin in vivo.
Elsasser, T. H., Fayer, R., Rumsey, T. S., et al. (1994) · Endocrinology · doi:10.1210/endo.134.3.8119146 · Cited by 49
Intracellular signaling mechanisms of sex hormones in acute myocardial inflammation and injury
Daniel, R. M. (2005) · Frontiers in bioscience · doi:10.2741/1665 · Cited by 49
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Background
Hematopoietic Stem-Progenitor Cells Restore Immunoreactivity and Improve Survival in Late Sepsis
Brudecki, L. E., Ferguson, D. A., Yin, D., LeSage, G., McCall, C. E., & Gazzar, M. E. (2011) · Infection and Immunity · doi:10.1128/iai.05480-11 · Cited by 48
“Anti-inflammatory treatment modalities targeting inflammatory mediators and bacterial toxins during the acute phase of sepsis were often effective in animal models of sepsis (44, 57) but failed in human clinical trials (26, 27, 49).”
Background
Estimate of CRP and TNF-alpha level before and after periodontal therapy in cardiovascular disease patients
Koppolu, P., Durvasula, S., Palaparthy, R., Rao, M., Sagar, V., Reddy, S. K., & Swapna, L. A. (2013) · Pan African Medical Journal · doi:10.11604/pamj.2013.15.92.2326 · Cited by 48
“Investigators added to substantiate the link between sepsis and TNF by utilizing anti-TNF monoclonal antibodies to counteract the circulating TNF and thereby put off its adverse effects on cardiovascular system [10].”
Background
The keratinocyte-derived cytokine IL-7 increases adhesion of the epidermal T cell subset to the skin basement membrane protein laminin-5
Wagner, L. A., Brown, T. A., Gil, S. C. I., Frank, I., Carter, W., Tamura, R. N., & Wayner, E. A. (1999) · European Journal of Immunology · doi:10.1002/(sici)1521-4141(199908)29:08 · Cited by 25
Inhibition of Nitric Oxide and Tumor Necrosis Factor-Alpha by Moutan Cortex in Activated Mouse Peritoneal Macrophages
Chung, H., Kang, M., Cho, C., Parvez, S., Park, C.-H., Kim, D., Oh, J., Kim, H., Shin, M., Hong, M., et al. (2007) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.30.912 · Cited by 48
Anti-Cytokine Therapies in Response to Systemic Infection
Dinarello, C. A. (2001) · Journal of Investigative Dermatology Symposium Proceedings · doi:10.1046/j.0022-202x.2001.00046.x · Cited by 47
The dynamics of cytokine d nitric oxide secretion in mice injected with Tityus serrulatus scorpion venom
Petricevich, V. L., & Peña, C. F. (2002) · Mediators of Inflammation · doi:10.1080/09622935020138811 · Cited by 48
“However, some coincidences or discrepancies were also observed in venom composition among several snakes and scorpions according to the age, sex, nutritional state and geographic regions where the animals were captured.(5,6) To minimize the experimental bias, mice strains were used to of Tityus serrulatus venom (TSV)…”
Method
Defects in Host Defense Mechanisms
van der Meer, J. W. M., & Kullberg, B. J. (2002) · Springer eBooks · doi:10.1007/0-306-47527-8_2 · Cited by 48
Alpha‐globulins suppress human leukocyte tumor necrosis factor secretion
Scuderi, P., Dorr, R. T., Liddil, J. D., Finley, P. R., Meltzer, P. S., Raitano, A. B., & Rybski, J. A. (1989) · European Journal of Immunology · doi:10.1002/eji.1830190523 · Cited by 48
Tumor Necrosis Factor and Interleukin 1 Appearance in Experimental Gram-negative Septic Shock
Busund, R. (1991) · Archives of Surgery · doi:10.1001/archsurg.1991.01410290067014 · Cited by 48
Is fatal pancreatitis a consequence of excessive leukocyte stimulation? The role of tumor necrosis factor α
Banks, R. E., Evans, S., Alexander, D. J., et al. (1991) · Cytokine · doi:10.1016/1043-4666(91)90004-w · Cited by 48
Tumor necrosis factor/cachectin. Induction of hemorrhagic necrosis in normal tissue requires the fifth component of complement (C5).
Rothstein, J. L., Lint, T. F., & Schreiber, H. W. (1988) · The Journal of Experimental Medicine · doi:10.1084/jem.168.6.2007 · Cited by 48
Definition of a Lipopolysaccharide-Responsive Element in the 5′-Flanking Regions of MuRantes and crg-2
Shin, H. S., Drysdale, B. E., Shin, M. L., Noble, P. W., Fisher, S. N., & Paznekas, W. A. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.5.2914 · Cited by 47
Cytokine–Ion Channel Interactions in Pulmonary Inflammation
Hamacher, J., Hadizamani, Y., Borgmann, M., Mohaupt, M. G., Männel, D. N., Moehrlen, U., Lucas, R., & Stammberger, U. M. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01644 · Cited by 48
“TNF − Disruption of the lung vascular barrier (236, 237)”
Background
Thalidomide protects mice against LPS-induced shock
Moreira, A. L., Wang, J., Sarno, E. N., & Kaplan, G. (1997) · Brazilian Journal of Medical and Biological Research · doi:10.1590/s0100-879x1997001000010 · Cited by 47
Adrenomedullin and adrenomedullin-binding protein-1 downregulate inflammatory cytokines and attenuate tissue injury after gut ischemia-reperfusion
Carrizo, G. J., Wu, R., Cui, X., et al. (2006) · Surgery · doi:10.1016/j.surg.2006.05.017 · Cited by 47
Protective effect of Aloe vera on polymicrobial sepsis in mice
Yun, N., Lee, C.-H., & Lee, S. (2009) · Food and Chemical Toxicology · doi:10.1016/j.fct.2009.03.013 · Cited by 48
“These results were also supported by data from several other groups including Tracey et al. (1987).”
Result
Antibiotics modulate the stimulated cytokine response to endotoxin in a human ex vivo, in vitro model
Ziegeler, S., Raddatz, A., Hoff, G., et al. (2006) · Acta Anaesthesiologica Scandinavica · doi:10.1111/j.1399-6576.2006.01112.x · Cited by 47
“Although this seems to be valid for the regional defence against bacterial stimuli, in systemic infection, an antiinflammatory regimen can be beneficial (22).”
Background
Is pyruvate an endogenous anti-inflammatory molecule?
Das, U. N. (2006) · Nutrition · doi:10.1016/j.nut.2006.05.009 · Cited by 47
“Sudden overproduction of tumor necrosis factor-alpha; TNF- ) occurs in acute septic shock and triggers hypotenion, circulatory collapse, renal and hepatic failures, and idespread inflammation and injury [3,4].”
Background
THE ROLE OF TUMOUR NECROSIS FACTOR-α IN THE PATHOGENESIS OF COMPLICATED FALCIPARUM MALARIA
Odeh, M. (2001) · Cytokine · doi:10.1006/cyto.2001.0845 · Cited by 47
Increased Release of Soluble Tumor Necrosis Factor Receptors Into Blood During Clinical Sepsis
Ertel, W. (1994) · Archives of Surgery · doi:10.1001/archsurg.1994.01420360120017 · Cited by 47
Vascular cell adhesion molecule–1 expression is obligatory for endotoxin-induced myocardial neutrophil accumulation and contractile dysfunction
Raeburn, C. D., Calkins, C. M., Zimmerman, M. A., Song, Y., Ao, L., Banerjee, A. M., Meng, X., & Harken, A. H. (2001) · Surgery · doi:10.1067/msy.2001.116410 · Cited by 45
Tumor Necrosis Factor Activity Increases in the Early Response to Trauma
Ferguson, K. L., Taheri, P. A., Rodriguez, J., et al. (1997) · Academic Emergency Medicine · doi:10.1111/j.1553-2712.1997.tb03676.x · Cited by 47
Induction of Tumor Necrosis Factor- in Murine Candida albicans Infection
Allendoerfer, R., Magee, D. M., Smith, J. G., Bonewald, L. F., & Graybill, J. R. (1993) · The Journal of Infectious Diseases · doi:10.1093/infdis/167.5.1168 · Cited by 47
Characterization of T-Cell Clones Derived From Peripheral Blood Lymphocytes of a Patient With Transfusion-Associated Graft-Versus-Host Disease: Fas-Mediated Killing by CD4+ and CD8+ Cytotoxic T-Cell Clones and Tumor Necrosis Factor β Production by CD4+ T-Cell Clones
Nishimura, M., Uchida, S., Mitsunaga, S., Yahagi, Y., Nakajima, K., Tadokoro, K., & Juji, T. (1997) · Blood · doi:10.1182/blood.v89.4.1440 · Cited by 44
Serum levels of tumor necrosis factor determine the fatal or non-fatal course of endotoxic shock
Mózes, T., Ben‐Efraim, S., Tak, C. A. M., et al. (1991) · Immunology Letters · doi:10.1016/0165-2478(91)90144-y · Cited by 47
The role of tumour necrosis factor‐α in acquired immunodeficiency syndrome
Odeh, M. (1990) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.1990.tb00278.x · Cited by 45
ARF6 Inhibition Stabilizes the Vasculature and Enhances Survival during Endotoxic Shock
Davis, C. T., Zhu, W., Gibson, C. C., Bowman-Kirigin, J. A., Sorensen, L. K., Jing, L., Sun, H., Navankasattusas, S., & Li, D. Y. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1400309 · Cited by 42
Aqueous ethanol extract of the fruit of Xylopia aethiopica (Annonaceae) exhibits anti-anaphylactic and anti-inflammatory actions in mice
Obiri, D. D., & Osafo, N. (2013) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2013.05.047 · Cited by 45
“Tumour necrosis factor alpha, TNFα, a cytokine produced by macrophages during septic shock is one of the endogenous mediators that cause cardiovascular injury and death (Tracey et al., 1986, 1987).”
Background
OxHDL controls LOX-1 expression and plasma membrane localization through a mechanism dependent on NOX/ROS/NF-κB pathway on endothelial cells
Pérez, L., Vallejos, A., Echeverría, C., Varela, D., Cabello‐Verrugio, C., & Simón, F. (2019) · Laboratory Investigation · doi:10.1038/s41374-018-0151-3 · Cited by 46
Effects of sesamin-supplemented dietary fat emulsions on the ex vivo production of lipopolysaccharide-induced prostanoids and tumor necrosis factor α in rats
Utsunomiya, T., Chavali, S. R., Zhong, W. W., et al. (2000) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/72.3.804 · Cited by 46
“Dietary PUFAs can influence the production of cytokines (22, 23), and overproduction of TNF- is associated with an increase in mortality during sepsis (24, 25).”
Background
Current status of Interleukin-2 therapy in cancer
Tartour, É., Mathiot, C., & Fridman, W. H. (1992) · Biomedicine & Pharmacotherapy · doi:10.1016/0753-3322(92)90005-r · Cited by 46
Macrophage migration inhibitory factor is a neuroendocrine mediator of endotoxaemia
Bernhagen, J., Calandra, T., Cerami, A., & Bucala, R. (1994) · Trends in Microbiology · doi:10.1016/0966-842x(94)90111-h · Cited by 46
Self-citation
Lead enhances lipopolysaccharide and tumor necrosis factor liver injury.
Honchel, R., Marsano, L. S., Cohen, D. A., Shedlofsky, S. I., & McClain, C. J. (1991) · PubMed · Cited by 46
Continuing Challenges of Sepsis Research
Crowther, M. (2001) · JAMA · doi:10.1001/jama.286.15.1894 · Cited by 46
LUNG-LIVER INTERACTIONS IN SEPSIS AND MULTIPLE ORGAN FAILURE SYNDROME
Matuschak, G. M. (1996) · Clinics in Chest Medicine · doi:10.1016/s0272-5231(05)70300-2 · Cited by 43
B cell-derived acetylcholine promotes liver regeneration by regulating Kupffer cell and hepatic CD8+ T cell function
Modares, N. F., Hendrikse, L. D., Smith, L. K., Paul, M. S., Haight, J., Luo, P., Liu, S., Fortin, J., Tong, F. K., Wakeham, A. C., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.04.002 · Cited by 29
Neutralization of TNF does not influence endotoxininduced changes in thyroid hormone metabolism in humans
van der Poll, T., Endert, E., Coyle, S. M., Agosti, J. M., & Lowry, S. F. (1999) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1999.276.2.r357 · Cited by 27
“Endogenous TNF has been implicated as an important mediator of LPS-induced host responses (26, 29, 30).”
BackgroundSelf-citation
Therapy with antibody to tumor necrosis factor in sepsis
Pennington, J. E. (1993) · Clinical Infectious Diseases · doi:10.1093/clinids/17.supplement_2.s515 · Cited by 26
“[25] can protect against sepsis due to either gram-positive or gram-negative bacteria.”
BackgroundInfluential

Authors: Tracey, K. J., Fong, Y., Hesse, D. G., Manogue, K. R., Lee, A. T., Kuo, G. C., Lowry, S. F., & Cerami, A.
Affiliations: Cornell University (US)
Rockefeller University (US)
ORCID: Tracey, Kevin J.
Fong, Yuman
Kuo, George C.
Cerami, Anthony
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1987-12
Volume: 330
Issue: 6149
Pages: 662-664
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/330662a0
OpenAlex: W2038434279
Cited by: 2,448
References: 1
Citations by year: 2026: 10 · 2025: 13 · 2024: 19 · 2023: 17 · 2022: 13 · 2021: 24 · 2020: 24 · 2019: 32 · 2018: 31 · 2017: 24 · 2016: 40 · 2015: 33 · 2014: 44 · 2013: 43 · 2012: 46
FWCI: 95.90
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: TNF-α, septic shock, bacteremia, Escherichia coli, passive immunization, neutralizing monoclonal antibodies, F(ab')2 fragments, endotoxic shock, organ failure, renal failure, respiratory failure, stress hormones, baboons, sepsis treatment
MeSH terms: Animals, Antibodies, Monoclonal, Blood Pressure, Cardiac Output, Catecholamines, Glucagon, Immunization, Passive, Immunologic Techniques, Leukocyte Count, Papio, Shock, Septic, Tumor Necrosis Factor-alpha, Sepsis

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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

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