Relationship of Endotoxin to Tumor Necrosis Factor–α and Interleukin-1β in Children with Otitis Media with Effusion

1998 ◽  
Vol 107 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Darryl N. Willett ◽  
Rod P. Rezaee ◽  
John M. Billy ◽  
Mary B. Tighe ◽  
Thomas F. DeMaria
Keyword(s):  
Otitis Media ◽  
Total Protein ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Otitis Media With Effusion ◽  
Chronic Otitis Media ◽  
Tnf Α ◽  
Factor Α ◽  
Mean Concentration ◽  
Necrosis Factor

Sixty-five middle ear effusions and paired sera from 41 children with chronic otitis media with effusion were assayed for endotoxin and for tumor necrosis factor–α (TNF-α) and interleukin-1β (IL-1β) in order to establish whether a correlation exists between the concentrations of endotoxin and of these cytokines. Endotoxin concentration was determined by means of a chromogenic limulus amebocyte lysate assay, and the cytokine concentration by means of a quantitative enzyme-linked immunosorbent assay. Forty percent of the effusions had detectable levels of endotoxin, with a mean concentration of 2.9 ± 7.8 endotoxin units per milligram of total protein. The mean concentration of TNF-α was 1.24 ± 3.1 pg/mg total protein, and that of IL-1β was 18.79 pg/mg total protein. A strong, statistically significant correlation exists between the concentrations of endotoxin and TNF-α (r =.89) and IL-1β (r =.72). The data indicate that endotoxin may contribute to the pathogenesis of chronic otitis media with effusion by stimulating the sustained production of TNF-α and IL-1β in the middle ear.

Tumor necrosis factor-α and interleukin-1 β levels in recurrent and persistent otitis media with effusion

2002 ◽  
Vol 126 (4) ◽  
pp. 417-422 ◽  
Author(s):  
Sertac Yetiser ◽  
Bulent Satar ◽  
Atilla Gumusgun ◽  
Faruk Unal ◽  
Yalcin Ozkaptan
Keyword(s):  
Tumor Necrosis Factor ◽  
Otitis Media ◽  
Tumor Necrosis ◽  
Otitis Media With Effusion ◽  
Interleukin 1 ◽  
Tertiary Referral Center ◽  
Adenoid Tissue ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

OBJECTIVE: Based on interleukin (IL)-1β and tumor necrosis factor (TNF)-α levels in effusions, our goals were to specify either recurrent or persistent otitis media with effusion (OME) is a mid stage in the development of chronic disease and to identify the factors that have an influence on cytokine levels. STUDY DESIGN: Samples from groups with recurrent (n = 15) and persistent (n = 39) OME were essayed for IL-1 β and TNF-α. Children were also grouped with respect to age, sex, quality of effusion, and the presence of pharyngeal adenoid tissue. SETTING: Tertiary referral center. RESULTS: In recurrent and persistent OME groups, IL-1β was higher than TNF-α ( P < 0.01). IL-β was higher in recurrent OME than in persistent OME ( P < 0.05). CONCLUSION: Recurrent OME seems to be closer to the chronic stage of the disease relative to persistent OME in terms of higher IL-1 β levels. Each exacerbation of acute disease in recurrent otitis media is likely to be mediated by IL-1 β. SIGNIFICANCE: We were able to clarify that recurrent OME is a stage that occurs before chronic OME. Therefore, the prevention of acute attacks in recurrent disease would also impede long-term damage to the middle ear.

Expression of Tumor Necrosis Factor-α, Interleukin-1α, Interleukin-6 and Interleukin-10 in Chronic Otitis Media with Bone Osteolysis

ORL ◽  
2011 ◽  
Vol 73 (2) ◽  
pp. 93-99 ◽  
Author(s):  
Jerzy Kuczkowski ◽  
Monika Sakowicz-Burkiewicz ◽  
Ewa Iżycka-Świeszewska ◽  
Bogusław Mikaszewski ◽  
Tadeusz Pawełczyk
Keyword(s):  
Tumor Necrosis Factor ◽  
Otitis Media ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Chronic Otitis Media ◽  
Interleukin 10 ◽  
Interleukin 1Α ◽  
Factor Α ◽  
Necrosis Factor

Determining Serum Haptoglobin and Proinflammatory Cytokines Concentration in the Calves Clinically Diagnosed with Pneumonitis, Pneumoenteritis and Enteritis

2021 ◽  
Author(s):  
M. Kabu ◽  
C. Uyarlar
Keyword(s):  
Tumor Necrosis Factor ◽  
Total Protein ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1 ◽  
Control Group ◽  
Serum Haptoglobin ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Background: This study aims to determine the concentration of serum haptoglobin (Hp), interleukin 1 (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) in cases of Pneumonia, Pneumoenteritis and Enteritis. Methods: 60 calves were subjected to the study and they were divided into four groups. The study group consisted of the claves diagnosed with clinical pneumonia (Group P; n=15), pneumoenteritis (Group PE; n=15) and enteritis (Group E; n=15) while the control group included the healthy calves (Group C; n=15). The measurements of the concentration of serum haptoglobin (Hp), interleukin 1 (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), Total protein (TP) and Albumin (ALB) were made by using commercial kits. Conclusion: In all infection groups (P, PE ve E), Haptoglobin concentration, serum cytokine (IL-1β, IL-6 and TNF-α) and Albumin values were found to have been higher than the control group (p≤0,005). However, there was no difference in total protein. In the light of these findings, it is suggested that routine controls for Haptoglobin and cytokine (IL-1β, IL-6 and TNF-α) concentrations would be rewarding to determine the severity of the infection, to choose the suitable treatment and to detect subclinical infections in veterinary medicine.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor α Inhibition for Alzheimer’s Disease

2017 ◽  
Vol 9 ◽  
pp. 117957351770927 ◽  
Author(s):  
Rudy Chang ◽  
Kei-Lwun Yee ◽  
Rachita K Sumbria
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Short Review ◽  
Tnf Α ◽  
Factor Α ◽  
Ad Therapy ◽  
Necrosis Factor

Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.

Tumor necrosis factor-α-associated lysosomal permeabilization is cathepsin B dependent

2002 ◽  
Vol 283 (4) ◽  
pp. G947-G956 ◽  
Author(s):  
Nathan W. Werneburg ◽  
M. Eugenia Guicciardi ◽  
Steven F. Bronk ◽  
Gregory J. Gores
Keyword(s):  
Tumor Necrosis Factor ◽  
Cathepsin B ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fluorescent Protein ◽  
Tnf Α ◽  
Calcein Release ◽  
Green Fluorescent ◽  
Factor Α ◽  
Necrosis Factor

Cathepsin B (Cat B) is released from lysososomes during tumor necrosis factor-α (TNF-α) cytotoxic signaling in hepatocytes and contributes to cell death. Sphingosine has recently been implicated in lysosomal permeabilization and is increased in the liver by TNF-α. Thus the aims of this study were to examine the mechanisms involved in TNF-α-associated lysosomal permeabilization, especially the role of sphingosine. Confocal microscopy demonstrated Cat B-green fluorescent protein and LysoTracker Red were both released from lysosomes after treatment of McNtcp.24 cells with TNF-α/actinomycin D, a finding compatible with lysosomal destabilization. In contrast, endosomes labeled with Texas Red dextran remained intact, suggesting lysosomes were specifically targeted for permeabilization. LysoTracker Red was released from lysosomes in hepatocytes treated with TNF-α or sphingosine in Cat B(+/+) but not Cat B(−/−) hepatocytes, as assessed by a fluorescence-based assay. With the use of a calcein release assay in isolated lysosomes, sphingosine permeabilized liver lysosomes isolated from Cat B(+/+) but not Cat B(−/−) liver. C6ceramide did not permeabilize lysosomes. In conclusion, these data implicate a sphingosine-Cat B interaction inducing lysosomal destabilization during TNF-α cytotoxic signaling.

Tumor Necrosis Factor-α −308 Genotypes Influence Inflammatory Activity and TNF-α Serum Concentrations in Children with Juvenile Idiopathic Arthritis

2009 ◽  
Vol 36 (4) ◽  
pp. 837-842 ◽  
Author(s):  
ANA FILIPA MOURÃO ◽  
JOANA CAETANO-LOPES ◽  
PAULA COSTA ◽  
HELENA CANHÃO ◽  
MARIA JOSÉ SANTOS ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inflammatory Activity ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Considering the relevance of tumor necrosis factor-α (TNF-α) in the pathophysiology of juvenile idiopathic arthritis (JIA), it is likely that polymorphisms in its promoter area may be relevant in disease susceptibility and activity. We investigated if clinical measures of JIA activity and TNF-α serum concentrations were associated with TNF-α −308 genotypes.Methods.Portuguese patients with JIA in 5 pediatric rheumatology centers were recruited consecutively, along with a control group of healthy subjects. Demographic and clinical data and blood samples were collected from each patient. DNA was extracted for analysis of TNF-α gene promoter polymorphisms at position −308 by restriction fragment-length polymorphism.Results.One hundred fourteen patients and 117 controls were evaluated; 57% of patients presented the oligoarticular subtype, 25% the polyarticular subtype, 8% the systemic subtype, and 9% had enthesitis-related arthritis and 5% psoriatic arthritis. Twenty-four percent of the patients presented the −308 GA/AA genotypes and 76% the −308 GG genotype, similar to findings in controls. Patients with the −308 GA/AA genotype had higher degree of functional impairment, erythrocyte sedimentation rate, 100-mm visual analog scale score for disease activity, and TNF-α levels compared to those with the −308 GG genotype.Conclusion.TNF-α −308 GA/AA genotypes were found to be related to higher inflammatory activity and worse measures of disease activity in Portuguese patients with JIA. They were not associated with susceptibility to JIA.

scholarly journals Tumor Necrosis Factor α Regulates Responses to Nerve Growth Factor, Promoting Neural Cell Survival but Suppressing Differentiation of Neuroblastoma Cells

2008 ◽  
Vol 19 (3) ◽  
pp. 855-864 ◽  
Author(s):  
Yoshinori Takei ◽  
Ronald Laskey
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Neuroblastoma Cells ◽  
Erk Activation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Although nerve growth factor (NGF) promotes survival of neurons, tumor necrosis factor α (TNF-α) contributes to cell death triggered by NGF depletion, through TNF-α receptor (TNFR) 1. In contrast to this effect, TNF-α can promote neural cell survival via TNF-α receptor TNFR2. Although these findings demonstrate pivotal roles of TNF-α and NGF in cell fate decisions, cross-talk between these signaling pathways has not been clarified. We find that NGF can induce TNF-α synthesis through the nuclear factor-κB transcription factor. This provides a new basis for examining the cross-talk between NGF and TNF-α. Inhibition of TNFR2 shows opposite effects on two downstream kinases of NGF, extracellular signal-regulated kinase (Erk) and Akt. It increases Erk activation by NGF, and this increased activation induces differentiation of neuroblastoma cell lines. Reciprocally, inhibition of TNFR2 decreases Akt activation by NGF. Consistent with an essential role of Akt in survival signaling, inhibition of TNF-α signaling decreases NGF-dependent survival of neurons from rat dorsal root ganglia. Thus, NGF and NGF-induced TNF-α cooperate to activate Akt, promoting survival of normal neural cells. However, the NGF-induced TNF-α suppresses Erk activation by NGF, blocking NGF-induced differentiation of neuroblastoma cells. TNFR2 signaling could be a novel target to modulate cell responses to NGF.

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