Differences of plasma IL-1 and TNF-α in healthy Chinese Population

AbstractPle iotropic proinflammatory cytokines, interleukin- 1 (IL-1) and tumor necrosis factor-α (TNF-α), involved in the regulations of various immune responses, inflammatory processes and hematopoiesis. In the present study, the expression levels of IL-1 and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA). Following the cytokine blockade as a successful clinical therapy for autoimm une diseases such as rheumatoid arthritis, the patients are more susceptible to a variety of opportunistic infections. IL-1 and TNF-α may be useful predictive biomarkers of diseases and offer potential targets for therapeutic intervention of inflammatory diseases. However, our results showed that the plasma IL-1 level was significantly higher in women compared to men (69.5 ± 19.8 pg/ ml in men and 80.1 ± 19.5 pg/ml in women, respectively); the plasma levels of TNF-α were higher in men than women (20.8 ± 4.9 pg/ml and 18.7 ± 7.1 pg/ml, respectively). The significant gender difference of plasma interleukin-1 (IL-1) and TNF-α levels present in healthy adults in Jiangsu Province, China (P=0.002 and P=0.015, respectively), and may be as a hint for sex differences of susceptibility to many diseases and elementary immune response.

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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽

10.3390/molecules25163573 ◽

2020 ◽

Vol 25 (16) ◽

pp. 3573

Author(s):

Lian-Chun Li ◽

Zheng-Hong Pan ◽

De-Sheng Ning ◽

Yu-Xia Fu

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Morphological Changes ◽

Raw264.7 Cells ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase ◽

Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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

Otolaryngology ◽

10.1067/mhn.2002.124188 ◽

2002 ◽

Vol 126 (4) ◽

pp. 417-422 ◽

Cited By ~ 7

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.

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Engineering Tumor Cells with Tumor Necrosis Factor α (TNF-α) or CD40 Ligand (CD40L) Genes Induce Anti-tumor Immune Responses

International Journal of Peptide Research and Therapeutics ◽

10.1007/s10989-018-9687-8 ◽

2018 ◽

Vol 25 (2) ◽

pp. 427-436

Author(s):

Saeed Daneshmandi ◽

Somayeh Shahrokhi

Keyword(s):

Tumor Necrosis Factor ◽

Immune Responses ◽

Tumor Cells ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Cd40 Ligand ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

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Predisposition to Hyperthyroidism May Be Influenced by Functional TNF-α, IL-1, IL-6, and IL-10 Polymorphisms: A Meta-Analysis

International Archives of Allergy and Immunology ◽

10.1159/000508284 ◽

2020 ◽

Vol 181 (12) ◽

pp. 956-965

Author(s):

Hong Ma ◽

Ting Tan ◽

Jie Wu ◽

Juan Chen ◽

Xiaohong Zhang

Keyword(s):

Meta Analysis ◽

Interleukin 1 ◽

Interleukin 10 ◽

Interleukin 4 ◽

Asian Origin ◽

Tnf Α ◽

Caucasian Origin ◽

Meta Analyses ◽

Factor Α ◽

Necrosis Factor

Background: Predisposition to hyperthyroidism may be influenced by functional gene polymorphisms in tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), and interleukin-10 (IL-10). However, the results of the studies published so far remain discrepant, so we conducted a meta-analysis to more robustly investigate relationships between TNF-α/IL-1/IL-4/IL-6/IL-10 polymorphisms and predisposition to hyperthyroidism. Methods: A comprehensive literature retrieval from PubMed, Embase, Web of Science, WanFang, VIP, and CNKI was endorsed by the authors, and 38 studies were found to be eligible for pooled meta-analyses. Results: We found that genotypic frequencies of TNF-α −308 G/A, IL-1A −889 C/T, IL-6 −174 G/C, IL-6 −572 G/C, IL-10 −819 C/T, and IL-10 −1082 A/G polymorphisms among cases were significantly different from those among controls. Moreover, we also found that genotypic frequencies of TNF-α −308 G/A and IL-6 −174 G/C polymorphisms among cases of Caucasian origin were significantly different from those among Caucasian controls, and genotypic frequencies of IL-1A −889 C/T, IL-1B −511 C/T, IL-6 −174 G/C, IL-6 −572 G/C, and IL-10 −1,082 A/G polymorphisms among cases of Asian origin were also significantly different from those among Asian controls. Conclusions: This meta-analysis suggests that TNF-α −308 G/A, IL-1A −889 C/T, IL-1B −511 C/T, IL-6 −174 G/C, IL-6 −572 G/C, IL-10 −819 C/T, and IL-10 −1,082 A/G polymorphisms may influence predisposition to hyperthyroidism in certain ethnic groups.

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The Augmented Productions of Neopterin and Cytokines from Macrophages/monocytes in vitro

Pteridines ◽

10.1515/pteridines.1996.7.3.72 ◽

1996 ◽

Vol 7 (3) ◽

pp. 72-76

Author(s):

Tadashi Lizuka ◽

Mitsuyo Sasaki ◽

Hitomi Kamisako ◽

Ko Oishi ◽

Shigeru Uemura ◽

...

Keyword(s):

Kawasaki Disease ◽

Interleukin 1 ◽

Poly I:C ◽

Recombinant Interferon ◽

Preliminary Examination ◽

Tnf Α ◽

Ifn Γ ◽

Factor Α ◽

Necrosis Factor

Summary In Kawasaki disease patients, increases in excretion of urinary neopterin coincided with fever and monocytosis in peripheral blood. We examined the products of neopterin, tumor necrosis factor-α (TNFα) and Interleukin-1 β (1L-1β) from healthy adult macrophages/monocytes (Mφ>/M), after stimulation with several activators to obtain some understanding of Kawasaki disease. Upon stimulation with either lipopolysaccharide (LPS) or polyinosinate-polycytidylate (Poly I:C), the Mφ/M released neopterin and pyogenic products (TNF-α or 1L-1β). The release of neopterin was eliminated by the addition of the anti-interferon-y antibody. The production of both TNF-α, 1L-1β and neopterin from Mφ/M upon stimulation of LPS was augmented in a co-culture with low dose recombinant interferon-y (rIFN-γ). Upon stimulation with rIFN-γ alone, however, the Mφ/M released neopterin but not the pyogenic products. A preliminary examination failed to detect. any difference in the response of the Mφ/M in adults annd children after stimulation with LPS. We concluded that some endotoxins could trigger the onset of Kawasaki disease and that endogenous IFN-γ can play an important role in the abnormality of Kawasaki disease patients

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Application of Dexmedetomidine in Cardiopulmonary Bypass Prefilling

Dose-Response ◽

10.1177/1559325820939764 ◽

2020 ◽

Vol 18 (3) ◽

pp. 155932582093976 ◽

Cited By ~ 1

Author(s):

Li Wang ◽

Shaowei Wang ◽

Zhen Xing ◽

Fulong Li ◽

Jinliang Teng ◽

...

Keyword(s):

Cardiopulmonary Bypass ◽

Cardiac Troponin ◽

Troponin I ◽

Serum Levels ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Anesthesia Induction ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

Objective: The purpose of this study was to explore the application of dexmedetomidine (Dex) in cardiopulmonary bypass. Methods: A total of 60 patients undergoing elective cardiopulmonary bypass were divided into control (C) group and Dex group. In the Dex group, appropriate amount of Dex was added into the membrane lung prefilling solution before anesthesia induction, while those in control group were given normal saline. The levels of mean arterial pressure (MAP) and heart rate (HR) at different times were measured. The levels of cardiac troponin I (CTNI), malondialdehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) at different points (T0/T1/T2/T3/T4) in both groups were measured by enzyme-linked immunosorbent assay kits. Results: The intraoperative and postoperative levels of MAP and HR in the 2 groups were significantly lower than those preoperatively ( P < .05). The levels of MAP and HR in the Dex group were significantly lower than those of the C group ( P < .05). The levels of CTNI/MDA/IL-6/TNF-α at different points in both groups were significantly higher than those at T0 ( P < .05). The serum levels of CTNI, MDA, IL-6, and TNF-α in the Dex group at T1/T2/T3/T4 were significantly lower than those in the C group ( P < .05). The rate of arrhythmia in the Dex group was significantly lower than that in the C group ( P < .05). Conclusion: Dexmedetomidine has a stable effect in cardiopulmonary priming solution.

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Induction of various cytokines and development of severe mucosal inflammation by cagA gene positive Helicobacter pylori strains

Gut ◽

10.1136/gut.41.4.442 ◽

1997 ◽

Vol 41 (4) ◽

pp. 442-451 ◽

Cited By ~ 240

Author(s):

Y Yamaoka ◽

M Kita ◽

T Kodama ◽

N Sawai ◽

K Kashima ◽

...

Keyword(s):

Helicobacter Pylori ◽

Expression Patterns ◽

Mucosal Inflammation ◽

Enzyme Linked Immunosorbent Assay ◽

Biopsy Specimens ◽

Tnf Α ◽

Polymerase Chain ◽

H Pylori ◽

Factor Α ◽

Necrosis Factor

Background—Helicobacter pyloristrains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8.Aims—To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).Patients and methods—In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1β, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor α (TNF-α) in antral biopsy specimens were measured by ELISA.Results—Mucosal levels of IL-1β, IL-6, IL-8, and TNF-α were significantly higher in H pyloripositive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1β and IL-8 were significantly higher in specimens infected with cagApositive strains than in those infected with cagAnegative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1β (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-α (p<0.0001).Conclusion—These findings suggest that the ability to induce cytokines differs among the strains;cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereascagA− strains induce IL-8 and IL-1β only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.

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Anti-tumor necrosis factor-α therapies attenuate adaptive arteriogenesis in the rabbit

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00959.2004 ◽

2005 ◽

Vol 289 (4) ◽

pp. H1497-H1505 ◽

Cited By ~ 40

Author(s):

Sebastian Grundmann ◽

Imo Hoefer ◽

Susann Ulusans ◽

Niels van Royen ◽

Stephan H. Schirmer ◽

...

Keyword(s):

Smooth Muscle ◽

Tumor Necrosis Factor ◽

Vascular Smooth Muscle ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Inflammatory Diseases ◽

Collateral Arteries ◽

Tnf Α ◽

Factor Α ◽

Necrosis Factor

The specific antagonists of tumor necrosis factor-α (TNF-α), infliximab and etanercept, are established therapeutic agents for inflammatory diseases such as rheumatoid arthritis and Crohn’s disease. Although the importance of TNF-α in chronic inflammatory diseases is well established, little is known about its implications in the cardiovascular system. Because proliferation of arteriolar connections toward functional collateral arteries (arteriogenesis) is an inflammatory-like process, we tested in vivo the hypothesis that infliximab and etanercept have antiarteriogenic actions. Sixty-three New Zealand White rabbits underwent femoral artery occlusion and received infliximab, etanercept, or vehicle according to clinical dosage regimes. After 1 wk, collateral conductance, assessed with fluorescent microspheres, revealed significant inhibition of arteriogenesis (collateral conductance): 52.4 (SD 8.1), 35.2 (SD 7.7), and 33.3 (SD 10.1) ml·min−1·100 mmHg−1 with PBS, infliximab, and etanercept, respectively ( P < 0.001). High-resolution angiography showed no significant differences in number of collateral arteries, but immunohistochemical analysis demonstrated a decrease in mean collateral diameter, proliferation of vascular smooth muscle cells, and reduction of leukocyte accumulation around collateral arteries in treated groups. Infliximab and etanercept bound to infiltrating leukocytes, which are important mediators of arteriogenesis. Infliximab induced monocyte apoptosis, and neither substance affected monocyte expression of the adhesion molecule Mac-1. We demonstrated that TNF-α serves as a pivotal modulator of arteriogenesis, which is attenuated by treatment with TNF-α inhibitors. Reduction of collateral conductance is most likely due to inhibition of perivascular leukocyte infiltration and subsequent lower vascular smooth muscle cell proliferation. This is the first report showing a negative influence of TNF-α inhibitors on collateral artery growth.

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BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy

10.21203/rs.3.rs-29090/v2 ◽

2020 ◽

Author(s):

Zetao Ma ◽

Deli Wang ◽

Jian Weng ◽

Sheng Zhang ◽

Yuanshi Zhang

Keyword(s):

Interleukin 1 ◽

Interleukin 1 Beta ◽

Related Protein ◽

Interacting Protein ◽

Tnf Α ◽

Adenovirus E1b ◽

Factor Α ◽

Related Proteins ◽

Necrosis Factor ◽

Proinflammatory Factors

Abstract Background: Inflammation and apoptosis of chondrocytes are the pathological basis of osteoarthritis. Autophagy could alleviate the symptoms of inflammation and apoptosis. Previous study has shown that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) can induce the occurrence and development of autophagy. However, it is unknown whether autophagy induced by BNIP3 can alleviate the inflammation and apoptosis of chondrocytes. Methods: We used the lentivirus to construct the overexpression BNIP3 chondrocytes. Next, the lipopolysaccharide (LPS) was used to stimulate these cells to simulate the physiological environment of osteoarthritis. After that, the enzyme-linked immunosorbent assays (ELISA) were performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) and the flow cytometry was performed to detect the apoptosis rates of chondrocytes. At last, the expression of autophagy related proteins was detected with the western blotting. Results: The expression of BNIP3 was suppressed after treatment with LPS. However, overexpression of BNIP3 inhibited the secretion of proinflammatory factors (TNF-α, IL-1β and IL-6) and decreased the apoptosis of chondrocytes. Furthermore, overexpression of BNIP3 led to the upregulation of autophagy related proteins expression including little computer 3 (LC3), autophagy-related protein 7 (ATG7) and Beclin-1. Application of autophagy inhibitor recovered the expression of proinflammatory factors and apoptosis rates of chondrocytes. Conclusions: BNIP3 decreased the LPS induced inflammation and apoptosis of chondrocytes by activating the autophagy.

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Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways

ASME 2007 Summer Bioengineering Conference ◽

10.1115/sbc2007-176541 ◽

2007 ◽

Author(s):

Valerie M. Wolfe ◽

Seonghun Park ◽

Marjana Tomic ◽

Peter A. Torzilli ◽

C. T. Christopher Chen

Keyword(s):

Inflammatory Responses ◽

Inflammatory Diseases ◽

Interleukin 1 ◽

Tensile Load ◽

Cartilage Degradation ◽

Acute Injury ◽

Cyclic Compression ◽

Tnf Α ◽

Necrosis Factor ◽

Pro Inflammatory Cytokines

Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.

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