Soluble tumor necrosis factor-alpha receptors in the serum of endometriosis patients

Human peripheral blood neutrophils (PMN) plated onto fibrinogen and activated with FMLP release H2O2 and lactoferrin, a specific granule component, with parallel kinetics. Although tumor necrosis factor-alpha (TNF alpha) only primes PMN in suspension, it is a potent agonist of adherent PMN. Activation of adherent PMN by FMLP (10(-7) mol/L) stimulated detectable release of TNF alpha within 45 minutes of stimulation, with maximal release (45.5 pg/10(6) cells) detected by 90 minutes. TNF alpha release paralleled the release of both lactoferrin and H2O2. To determine if TNF alpha plays a role in H2O2 and lactoferrin release, we investigated the effect of anti-TNF alpha antibodies on FMLP-stimulated activation of adherent PMN. A neutralizing rabbit anti-TNF alpha antibody inhibited both H2O2 and lactoferrin release stimulated by FMLP, whereas rabbit lgG, anti-HLA- A,B,C, anti-CD 14, and anti-interleukin-8 antibodies were without effect. The simultaneous addition of TNF alpha (1,000 U/mL) with anti- TNF alpha antibody reversed the inhibition seen with anti-TNF alpha alone. Furthermore, treatment of PMN with either actinomycin D or cylcoheximide resulted in partial (33%) inhibition of H2O2 and lactoferrin release, suggesting that protein synthesis is required for FMLP-mediated activation of adherent PMN. The addition of TNF alpha to either cycloheximide or of actinomycin D-treated PMN overcame the inhibition, indicating that the effect was specific for TNF alpha. The addition of antibodies against either the 55-or 75-kD TNF alpha receptors (referred to as p55 and p75, respectively) resulted in partial (32%) inhibition of FMLP-mediated activation of H2O2 and lactoferrin release, whereas a combination of both antibodies reduced their release to control levels. These data indicate that both p55 and p75 are involved in FMLP activation of adherent PMN. Taken together, these findings indicate that the production of TNF alpha and ligation of TNF alpha receptors are central to FMLP activation of PMN adherent to fibrinogen.

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Effect of six-month lifestyle intervention on adiponectin, resistin and soluble tumor necrosis factor-^|^alpha; receptors in obese adolescents

Endocrine Journal ◽

10.1507/endocrj.ej14-0157 ◽

2014 ◽

Vol 61 (9) ◽

pp. 921-931 ◽

Cited By ~ 11

Author(s):

Fengyang Huang ◽

Blanca Estela del-R^|^iacute;o-Navarro ◽

Jos^|^eacute; Alfredo P^|^eacute;rez-Ontiveros ◽

Eliseo Ruiz-Bedolla ◽

Omar Josu^|^eacute; Saucedo-Ram^|^iacute;rez ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Lifestyle Intervention ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Necrosis Factor Alpha ◽

Obese Adolescents ◽

Alpha Receptors ◽

Factor Alpha ◽

Necrosis Factor

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Tumor necrosis factor alpha (TNF alpha) downregulates c-kit proto- oncogene product expression in normal and acute myeloid leukemia CD34+ cells via p55 TNF alpha receptors

Blood ◽

10.1182/blood.v84.8.2506.bloodjournal8482506 ◽

1994 ◽

Vol 84 (8) ◽

pp. 2506-2514 ◽

Cited By ~ 2

Author(s):

E Khoury ◽

C Andre ◽

S Pontvert-Delucq ◽

B Drenou ◽

C Baillou ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Tnf Alpha ◽

Necrosis Factor Alpha ◽

Cd34 Cells ◽

Alpha Receptors ◽

Factor Alpha ◽

Necrosis Factor ◽

Acute Myeloid

Tumor necrosis factor alpha (TNF alpha), as a modulator of hematopoiesis, interacts with many growth factor receptors, such as interleukin-3, granulocyte-macrophage colony-stimulating factor (CSF), and granulocyte-CSF receptors. Here, we studied the interactions between TNF alpha and the stem cell factor (SCF) receptor, c-kit, in normal CD34+ hematopoietic progenitors and their leukemic counterpart, ie, acute myeloid leukemic (AML) CD34+ cells coexpressing c-kit antigen. The results showed that (1) incubation of normal bone marrow mononuclear cells with 200 U/mL rhTNF alpha for 20 hours induced a diminution of 31.2% +/- 5.2% of CD34+ cells coexpressing c-kit; (2) the same decrease was observed using purified CD34+ cells and, furthermore, their proliferative response to SCF was inhibited by 31.5% +/- 7.3% after exposure to TNF alpha; (3) similar experiments performed on CD34+ c-kit+ AML cells from 11 patients gave comparable results. Further analysis at the mRNA level indicated that TNF alpha decreased c-kit mRNA transcripts. Moreover, using monoclonal antibodies against the two types of TNF alpha receptors, p75 and p55, we showed that the downregulation of c-kit proto-oncogene product by TNF alpha, on normal and leukemic CD34+ cells, was exclusively mediated by the TNF alpha p55 receptor. Therefore, we conclude that TNF alpha acts as a downregulator of the SCF receptor expression.

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Association between serum soluble tumor necrosis factor-α receptors and early childhood obesity

Endocrine Journal ◽

10.1507/endocrj.ej15-0628 ◽

2016 ◽

Vol 63 (6) ◽

pp. 581-587 ◽

Cited By ~ 4

Author(s):

Shengrong Ouyang ◽

Wei Li ◽

Zhuo Liu ◽

Yuanyuan Li ◽

Sen Li ◽

...

Keyword(s):

Early Childhood ◽

Childhood Obesity ◽

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Necrosis Factor Alpha ◽

Alpha Receptors ◽

Early Childhood Obesity ◽

Factor Alpha ◽

Necrosis Factor

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Tumor necrosis factor alpha (TNF alpha) downregulates c-kit proto- oncogene product expression in normal and acute myeloid leukemia CD34+ cells via p55 TNF alpha receptors

Blood ◽

10.1182/blood.v84.8.2506.2506 ◽

1994 ◽

Vol 84 (8) ◽

pp. 2506-2514 ◽

Cited By ~ 23

Author(s):

E Khoury ◽

C Andre ◽

S Pontvert-Delucq ◽

B Drenou ◽

C Baillou ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Tnf Alpha ◽

Necrosis Factor Alpha ◽

Cd34 Cells ◽

Alpha Receptors ◽

Factor Alpha ◽

Necrosis Factor ◽

Acute Myeloid

Abstract Tumor necrosis factor alpha (TNF alpha), as a modulator of hematopoiesis, interacts with many growth factor receptors, such as interleukin-3, granulocyte-macrophage colony-stimulating factor (CSF), and granulocyte-CSF receptors. Here, we studied the interactions between TNF alpha and the stem cell factor (SCF) receptor, c-kit, in normal CD34+ hematopoietic progenitors and their leukemic counterpart, ie, acute myeloid leukemic (AML) CD34+ cells coexpressing c-kit antigen. The results showed that (1) incubation of normal bone marrow mononuclear cells with 200 U/mL rhTNF alpha for 20 hours induced a diminution of 31.2% +/- 5.2% of CD34+ cells coexpressing c-kit; (2) the same decrease was observed using purified CD34+ cells and, furthermore, their proliferative response to SCF was inhibited by 31.5% +/- 7.3% after exposure to TNF alpha; (3) similar experiments performed on CD34+ c-kit+ AML cells from 11 patients gave comparable results. Further analysis at the mRNA level indicated that TNF alpha decreased c-kit mRNA transcripts. Moreover, using monoclonal antibodies against the two types of TNF alpha receptors, p75 and p55, we showed that the downregulation of c-kit proto-oncogene product by TNF alpha, on normal and leukemic CD34+ cells, was exclusively mediated by the TNF alpha p55 receptor. Therefore, we conclude that TNF alpha acts as a downregulator of the SCF receptor expression.

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Interference of soluble TNF-alpha receptors in immunological detection of tumor necrosis factor-alpha

Clinical Chemistry ◽

10.1093/clinchem/42.9.1450 ◽

1996 ◽

Vol 42 (9) ◽

pp. 1450-1453 ◽

Cited By ~ 20

Author(s):

E Moreau ◽

J Philippé ◽

S Couvent ◽

G Leroux-Roels

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Tnf Alpha ◽

Necrosis Factor Alpha ◽

Alpha Receptors ◽

Clear Insight ◽

Factor Alpha ◽

Capture Antibody ◽

Necrosis Factor

Abstract We have studied the interference of soluble tumor necrosis factor-alpha receptor p55 (sTNF-R55) on the quantification of tumor necrosis factor-alpha (TNF-alpha) in three immunoassays: the commercially available enzyme amplified-sensitivity immunoassay (EASIA) of Medgenix and the ELISA of Boehringer Mannheim, and an assay based on electrochemiluminescence (ECL) technology. TNF-alpha measurements by EASIA and ELISA were not affected by the presence of sTNF-R55, but results by the ECL method were clearly influenced by the receptor. We then performed a second set of experiments with the ECL system to examine what factors might influence the importance of interference from sTNF-R55 and soluble TNF-alpha receptor p75 (sTNF-R75), which influences TNF-alpha measurements the same as sTNF-R55. We found that extending the incubation time and increasing the concentration of capture antibody decreased the interfering capacity of sTNF-R55 and sTNF-R75. A clear insight into these phenomena is of utmost importance for correct interpretation of cytokine quantification.

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