scholarly journals Association between tumor necrosis factor-α and chronic obstructive pulmonary disease: a systematic review and meta-analysis

2019 ◽  
Vol 13 ◽  
pp. 175346661986609 ◽  
Author(s):  
Yang Yao ◽  
Jing Zhou ◽  
Xin Diao ◽  
Shengyu Wang
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Meta Analysis ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Background: Patients diagnosed with chronic obstructive pulmonary disease (COPD) have increased risks for a series of physical and mental illnesses. Tumor necrosis factor-α (TNF-α) has been reported to participate in the development of COPD and its complications. However, the values of blood TNF-α level used in the diagnosis of COPD remains controversial. In view of this, we performed a systematic review and meta-analysis to evaluate the correlation between TNF-α level and COPD. Methods: We searched PubMed, Web of Science, Embase and CNKI up to May 2018. The selection criteria were set according to the PICOS framework. A random-effects model was then applied to evaluate the overall effect sizes by calculating standard mean difference (SMD) and its 95% confidence intervals (CIs). Results: A total of 40 articles containing 4189 COPD patients and 1676 healthy controls were included in this meta-analysis. The results indicated a significant increase in TNF-α level in the COPD group compared with the control group (SMD: 1.24, 95% CI: 0.78–1.71, p < 0.00001). According to the subgroup analyses, we noted that TNF-α level was associated with predicted first second of forced expiration (FEV1) (%) and study region. However, no association between TNF-α level and COPD was found when the participants were nonsmokers, and the mean age was less than 60 years. Conclusions: Our results indicated that TNF-α level was increased in COPD patients when compared with healthy controls. Illness progression and a diagnosis of COPD might contribute to higher TNF-α levels. However, the underlying mechanism still remains unknown and needs further investigation. The reviews of this paper are available via the supplemental material section.

The Role of Tumor Necrosis Factor-α (TNF-α) Polymorphisms in Gastric Cancer: a Meta-Analysis

2021 ◽  
Author(s):  
Maryam Gholamalizadeh ◽  
Samaneh Mirzaei Dahka ◽  
Hadi Sedigh Ebrahim-Saraie ◽  
Mohammad Esmail Akbari ◽  
Azam Pourtaheri ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Meta Analysis ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

scholarly journals The clinical significance of tumor necrosis factor-α plasma level in patients having chronic lymphocytic leukemia

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1215-1219 ◽  
Author(s):  
Alessandra Ferrajoli ◽  
Michael J. Keating ◽  
Taghi Manshouri ◽  
Francis J. Giles ◽  
Amanda Dey ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Lymphocytic Leukemia ◽  
Tnf Α ◽  
The Mean ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α), a cytokine possessing pleiotropic biological activities, is produced by leukemic lymphocytes in patients with chronic lymphocytic leukemia (CLL) and acts as an autocrine and paracrine growth factor in this disease. In this study, TNF-α levels were determined in 150 patients with CLL and correlated with disease characteristics, prognostic factors, and survival. The mean TNF-α plasma concentration in the patients with CLL was significantly higher than in the healthy control population (16.4 versus 8.7 pg/mL; P &lt; .0001). Patients having an elevated TNF-α level had more advanced Rai and Binet stage disease, higher serum β2-microglobulin (β2M) levels, a greater percentage of cells expressing CD38, and lower hemoglobin and platelet levels. Patients having chromosomal abnormalities such as 11q deletion, trisomy 12, and chromosome 17 aberrations had a higher mean TNF-α level (27.5 pg/mL) than patients having a diploid karyotype or other miscellaneous cytogenetic abnormalities (14.2 pg/mL;P &lt; .001). The TNF-α level was a predictor of survival when the Cox proportional hazards model was used with TNF-α entered as a continuous variable (P = .0001). Also, patients having a TNF-α level above the mean value of 14 pg/mL had significantly shorter survival duration (P = .00001). The TNF-α level remained predictive of survival in Cox multivariate analysis independent of Rai staging and β2M, hemoglobin, prior therapy, white cell count, and platelet level (P = .005). We conclude that the TNF-α level serves as a prognostic factor in patients with CLL and that inhibition of TNF-α in these patients could have therapeutic importance.

Evidence supporting involvement of leukotrienes in LPS-induced hypothermia in mice

1999 ◽  
Vol 276 (1) ◽  
pp. R52-R58 ◽  
Author(s):  
Lada Paul ◽  
Vadim Fraifeld ◽  
Jacob Kaplanski
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ex Vivo ◽  
Induced Hypothermia ◽  
Significant Elevation ◽  
Hypothermic Effect ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

The aim of the present study was to examine a possible involvement of leukotrienes (LTs) in lipopolysaccharide (LPS)-induced body temperature (Tb) response. We examined the effect of MK-886, an inhibitor of LT synthesis, on changes in Tb, plasma tumor necrosis factor-α (TNF-α), hypothalamic LT, and PGE2 production. Intraperitoneal injection of LPS (50 μg/mouse) led to a decrease in Tb starting 1 h after the injection. The hypothermic effect of LPS was accompanied by a significant elevation in TNF-α level in plasma and in LT and PGE2 production by ex vivo-incubated hypothalamus. MK-886 (1 mg/kg ip) administered 4 h before LPS efficaciously prevented LPS-induced hypothermia in mice. Pretreatment of mice with MK-886 did not alter the LPS-stimulated increase in plasma TNF-α. MK-886 significantly inhibited LT and enhanced PGE2 production in hypothalamus compared with LPS alone. These results suggest that 1) LPS-induced hypothermia may be mediated by LTs and 2) the antihypothermic effect of MK-886 is not associated with TNF-α bioactivity.

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