Clinical Immunology and Immunopathology
Short analytical reviewTumor necrosis factor in the pathophysiology of infection and sepsis☆
References (84)
- et al.
Raised levels of tumor necrosis factor in parasitic infections
Lancet
(1986) - et al.
Association between tumor necrosis factor in serum and fatal outcome in patients with meningococcal disease
Lancet
(1987) - et al.
Evidence for tumor necrosis factor/cachectin production in cancer
Lancet
(1987) - et al.
Correlation of plasma interleukin 1 levels with disease activity in rheumatoid arthritis
Lancet
(1988) - et al.
A novel form of TNF/cachectin is a cell surface cytotoxic transmembrane protein: Ramifications for the complex physiology of TNF
Cell
(1988) - et al.
Tumor necrosis factor stimulates IL-1 and PGE2 production in resting macrophages
Biochem. Biophys. Res. Commun.
(1986) - et al.
Cachectin/tumor necrosis factor
Lancet
(1989) - et al.
Hepatocellular membrane function during chronic burn injury
J. Surg. Res.
(1989) - et al.
Weight loss associated with an endotoxin-induced mediator from peritoneal macrophages: The role of cachectin (tumor necrosis factor)
Immunol. Lett.
(1985) - et al.
Tumor secreting human TNF/cachechin induce cachexia in mice
Cell
(1987)
Biology of cachectin
Cachectin and tumor necrosis factor as two sides of the same biologic coin
Nature (London)
Studies of endotoxin-induced decrease in lipoprotein lipase activity
J. Exp. Med.
Identity of tumor necrosis factor and the macrophage secreted factor cachectin
Nature (London)
Cachectin/tumor necrosis-factor production by cancer patients
Lancet
Raised serum levels of cachectin/tumor necrosis factor alpha in renal allograft rejection
J. Exp. Med.
Cachectin/TNF production in experimental burns and Pseudomonas infection
Arch. Surg.
Participation of tumor necrosis factor in the mediation of gram negative bacterial lipopolysaccharide-induced injury in rabbits
J. Clin. Invest.
Cachectin/tumor necrosis factor: Production, distribution, and metabolic fate in vivo
J. Immunol.
Cytokine appearance in human endotoxemia and primate bacteremia
Surg. Gynecol. Obstet.
Splanchnic monokine and metabolic response to endotoxin in man
Surg. Forum
Differential host responses to repeated LPS administration: Correlates to plasma TNF and IL-6 levels
Cytokine
Antibodies to cachectin/TNF reduces interleukin-1β and interleukin-6 appearance during lethal bacteremia
J. Exp. Med.
Cachectin/tumor necrosis factor mediates changes of skeletal muscle plasma membrane potential
J. Exp. Med.
Phase I study of recombinant tumor necrosis factor in cancer patients
Cancer Res.
Syngergy between tumor necrosis factor and bacterial products causes hemorrhagic necrosis and lethal shock in normal mice
Modulation of endogenous hormone action by recombinant human tumor necrosis factor
Role of interleukin 1 and tumor necrosis factor on energy metabolism in rabbits
Amer. J. Physiol.
Growth inhibition of Candida albicans by human polymorphonuclear neutrophils: Activation by interferon-g and tumor necrosis factor
J. Immunol.
Cachectin/tumor necrosis factor gene expression in kupffer cells
J. Leukocyte Biol.
Control of cachectin (tumor necrosis factor) synthesis: Mechanism of endotoxin resistance
Science
Cachectin: More than a tumor necrosis factor
N. Engl. J. Med.
Endotoxin-induced cytokine gene expression in vivo
Amer. J. Pathol.
Compartmentalization of intraalveolar and systemic lipopolysaccharide-induced tumor necrosis factor and pulmonary inflammatory response
J. Infect. Dis.
Tumor necrosis factor α in cerebrospinal fluid during bacterial, but not viral, meningitis
J. Exp. Med.
Multiple forms of in serum and body fluids during acute bacterial infection
J. Immunol.
Characterization of wound cytokine in the sponge matrix model
Arch. Surg.
Membrane-associated interleukin-1α as a mediator of tumor killing by human blood monocytes fixed with paraformaldehyde
Cancer Res.
Endotoxemia elicits increased circulating in man
J. Immunol.
Cited by (214)
Arid5a, an RNA-Binding Protein in Immune Regulation: RNA Stability, Inflammation, and Autoimmunity
2020, Trends in ImmunologyCitation Excerpt :By contrast, Arid5a-/- mice are resistant to P. acnes-primed LPS injection; it has been proposed that in this model, Arid5a regulates increases in IFN-γ and IL-6 expression via the stabilization of Tbx21 and Il6 mRNAs, respectively, and possibly synergistically amplify the expression of various other cytokines that ultimately lead to the development of septic shock in mice (Figure 4) [3]. For instance, other cytokines, such as IL-1, act synergistically with TNF-α, stimulating the release of mediators such as IL-6, IL-8, IL-10, IL-13, and TGF-β, which participate in the host inflammatory response and the pathogenesis of sepsis and septic shock [64–67]. Thus, antagonistic agents targeting Arid5a expression might prove to be beneficial in the prevention/control of certain pathological outcomes of sepsis, although this remains to be rigorously tested.
Cytokines and Inflammatory Response in the Fetus and Neonate
2011, Fetal and Neonatal Physiology E-Book, Fourth EditionEffect of GLC756, a novel mixed dopamine D1 receptor antagonist and dopamine D2 receptor agonist, on TNF-alpha release in vitro from activated rat mast cells
2006, Experimental Eye ResearchCitation Excerpt :However, a recent in vitro study in which the inflammatory potential of the prostaglandin analogues latanoprost, travoprost, and bimatoprost in conjunctiva-derived epithelial cells was tested revealed no increase of the inflammation markers intercellular adhesion molecule (ICAM)-1, platelet-endothelial cell adhesion molecule (PECAM)-1 and HLA DR (Guenoun et al., 2005). This is consistent with the results of the present in vitro study, where latanoprost did not significantly modify TNF-α release from activated RBL-2H3 mast cells, which is one of the first cytokines released in the cascade of processes leading to inflammation (Fong and Lowry, 1990). In the case of timolol, no significant effect on TNF-α release from activated mast cells was detected in the concentration range 0.1–30 μM suggesting that this antiglaucoma drug can not alleviate or possibly could aggravate allergic conjunctivitis of antiglaucoma medicated patients.
Exogenous testosterone modulates tumor necrosis factor-α and acute phase protein responses to repeated endotoxin challenge in steers
2006, Domestic Animal EndocrinologyGLC756 decreases TNF-α via an alpha2 and beta2 adrenoceptor related mechanism
2006, Experimental Eye ResearchCitation Excerpt :Apoptosis has been implicated in the death of retinal ganglion cells (Quigley et al., 1995) and there is evidence that apoptosis-promoting substances, including TNF-α secreted by activated glial cells after exposure to stress, contribute directly to neuronal cytotoxicity. Since TNF-α is a mediator of inflammation (Fong and Lowry, 1990; Durum and Oppenheim, 1989) and plays a role in apoptotic processes (Tezel and Wax, 2000) it is possible that compounds that prevent TNF-α production such as GLC756 have anti-inflammatory and neuroprotective properties which represents an additional benefit for the treatment of glaucoma. Because the pharmacological profile of GLC756 is very complex the elucidation of the mechanism of action of its TNF-α decreasing effect is not easy.
- ☆
Supported in part by Grant K04GM-00505 and GM-34695 from the National Institutes of Health, Bethesda, Maryland.