Evidence for different effects of soluble TNF-receptors on various TNF measurements in human biological fluids

Engelberts, I.; Stephens, Sue; Francot, Gaby J. M.; Linden, C. J. Van Der; Buurman, Wim A.

doi:10.1016/0140-6736(91)90591-c

Cited by 150 publications

(66 citation statements)

References 8 publications

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“…Since the presence of TNF-sR55 or TNF-sR75 did not impede TNFa determination in the radioimmunoassay (ref. 12 and Grau G, University of Geneva: personal communication), the low TNFa levels in SF could not be due to interference with the soluble receptors. It is more likely that following a transient increase in TNFa synthesis-undetected because of the short half-life of TNFa-an elevation of TNF-sR concentrations may ensue and persist for prolonged periods.…”

Section: Discussionmentioning

confidence: 93%

Soluble tumor necrosis factor receptors in human inflammatory synovial fluids

Roux‐Lombard

Punzi

Hasler

et al. 1993

Arthritis & Rheumatism

119

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Objective. To test synovial fluid (SF) for the presence of soluble fragments originating from distinct tumor necrosis factor receptors (TNF-sR55 and TNFsR75) which bind to TNF and inhibit its biologic activity.Methods. TNF-sR55 and TNF-sR75 were measured in 62 SF samples by specific immunoassays using monoclonal antibodies.Results. Both TNF-sR were present in all of the SF tested. Their concentrations were higher in SF from patients with seropositive rheumatoid arthritis than in patients with other inflammatory arthritides. The relative amount of TNF-sR75, as compared with TNF-sR55, was higher in seropositive RA SF than in other SF. Conclusion. The balance between TNF and its

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Section: Discussionmentioning

confidence: 93%

Soluble tumor necrosis factor receptors in human inflammatory synovial fluids

Roux‐Lombard

Punzi

Hasler

et al. 1993

Arthritis & Rheumatism

119

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“…Following surgery, only TT<F-sR55 became significantly elevated in all three groups above baseline in the first 48 h. The failure to detect significant levels of TNF-a in any ofthe three groups would suggest that TNF-sR, in addition to being antagonistic to the effects of TNF-a, may have a potential TNF-a-buffering capacity. It should be noted that presently available commercial kits are unable to detect TNF-a when hound to TNF-sR [33], whieh supports this 'buffering' concept. f urther indirect evidence to support this hypothesis comes from the observations that cancer patients receiving a 60-min infusion of human recombinant TNF-a show a transient increase in circulating TNF-sR within 30-120 min coinciding with peak levels of TNF-a; [34] and that production of TNF-sR is also increased during endotoxaemia and meningococcaemia [25,35].…”

Section: Discussionmentioning

confidence: 93%

“…and this has been attributed to the presence of TNF-sR [33]. TNF-sR bebave like acute phase reactants: first, the levels of TNF-SR55 and TNF-sR75 were identical in RA and OM subjects over a 24-h period and were significantly higher than in NIA; second, TNF-sR55 increased early following surgery in RA.…”

Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis

Chikanza

Roux‐Lombard

Dayer

et al. 1993

Clinical and Experimental Immunology

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SUMMARY Tumour necrosis factor‐alpha (TNF‐α) is involved in diverse biological processes including immune and inflammatory reactions and the response to surgical stress. Two soluble TNF receptor protein fragments. TNF‐sR55 (from the p55 kD TNF receptor) and TNF‐sR75 (from the p75 kD TNF receptor), are released by cells during inflammation and may modulate the effects of TNF‐α. We have studied the kinetics of secretion of TNF‐α, TNF‐sR55 and TNF‐sR75 in the sera of patients with rheumatoid arthritis (RA) and control subjects with osteoarthritis (OA) or chronic osteomyelitis (OM) before and after major surgery. Significantly higher pre‐operative levels of TNF‐sR55 and TNF‐sR75 were found in RA and OM as compared with OA (P<0.02). Following surgery, TNF‐sR55 increased within 24 h in RA, OM and OA (P<0.05), whereas TNF‐sR75 increased significantly only in OM and OA patients (P<0.05). By contrast, no TNF‐α was detectable before and after surgery in any of the subjects, but this may have been due to impaired detection (by ELISA) of TNF‐α when it is bound to TNF‐sR. These findings suggest that TNF‐sR55 and TNF‐sR75 may be further markers of the host's reaction to inflammatory insults. They may also play a role in modulating the immune and inflammatory reactions by inhibiting the systemic effects of TNF‐α.

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“…The serum concentrations of TNF were determined by an assay (IRMA; Medgenix, Fleurus, Belgium). This assay measures TNF regardless of whether it is complexed with its soluble receptors and is therefore not disturbed by high circulating concentrations of sTNFRs [25].…”

Section: Methodsmentioning

confidence: 99%

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Poll

Jansen²,

Leenen³

et al. 1993

Journal of Infectious Diseases

115

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To assess the role of tumor necrosis factor (TNF) in the appearance of soluble TNF receptors (sTNFRs), 20 consecutive patients with a clinical diagnosis of sepsis were studied as were 7 chimpanzees after administration of endotoxin (4 ng/kg) with or without pentoxifylline. The patients had markedly elevated serum levels of sTNFR-p55 and sTNFR-p75 compared with healthy controls (P < .0001 for both receptors). The levels of both soluble receptors correlated with simultaneously measured immunoreactive TNF concentrations (p55: r = .63, P < .01; p75: r = .69, P < .001). In the chimpanzees, endotoxin induced subsequent rises in the serum concentrations ofTNF and sTNFRs. Although pentoxifylline reduced the TNF response to intravenous endotoxin to 20% (P < .05), the appearance of sTNFRs was only moderately inhibited (sTNFRp55 to 79% on average, P < .05; sTNFR-p75 to 77%, P = .12). These results indicate that TNF either does not play an important role in the appearance of sTNFRs in systemic infection or that a small amount of TNF remaining in the circulation after some bacterial challenges is sufficient to preserve the secretion of its soluble receptors.Sepsis is a syndrome characterized by hypotension, vascular leakage, and failure of multiple organs. Tumor necrosis factor (TNF) is an important factor for initiation ofthe septic syndrome [1 ]. Massive induction ofTNF synthesis, resulting in high concentrations of the protein in the circulation, is a prerequisite for the development of shock and multiple organ failure in experimental sepsis in animals [2]. In patients with sepsis, the extent of systemic TNF release correlates strongly with mortality rates [3,4]. Administration of TNF to animals or humans reproduces many of the features of septicemia [5,6]. Recently, naturally occurring inhibitors of TNF activity have been found in the urine of normal individuals and febrile patients and in the serum of patients with renal insufficiency [7][8][9][10][11]. These host mediators, originally termed TNF-binding proteins, have subsequently been identified as the soluble extracellular domains of the 55-and 75-kDa membrane-bound TNF receptors [12][13][14][15][16]. Soluble

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Evidence for different effects of soluble TNF-receptors on various TNF measurements in human biological fluids

Cited by 150 publications

References 8 publications

Soluble tumor necrosis factor receptors in human inflammatory synovial fluids

Soluble tumor necrosis factor receptors in human inflammatory synovial fluids

Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

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