Journal articles on the topic 'Tumor Necrosis Factor Alpha α-SMA'
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1
Sullivan, K. E., A. B. M. Reddy, K. Dietzmann, A. R. Suriano, V. P. Kocieda, M. Stewart, and M. Bhatia. "Epigenetic Regulation of Tumor Necrosis Factor Alpha." Molecular and Cellular Biology 27, no. 14 (May 21, 2007): 5147–60. http://dx.doi.org/10.1128/mcb.02429-06.
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ABSTRACT Tumor necrosis factor alpha (TNF-α) is a potent cytokine which regulates inflammation via the induction of adhesion molecules and chemokine expression. Its expression is known to be regulated in a complex manner with transcription, message turnover, message splicing, translation, and protein cleavage from the cell surface all being independently regulated. This study examined both cell lines and primary cells to understand the developmental regulation of epigenetic changes at the TNF-α locus. We demonstrate that epigenetic modifications of the TNF-α locus occur both developmentally and in response to acute stimulation and, importantly, that they actively regulate expression. DNA demethylates early in development, beginning with the hematopoietic stem cell. The TNF-α locus migrates from heterochromatin to euchromatin in a progressive fashion, reaching euchromatin slightly later in differentiation. Finally, histone modifications characteristic of a transcriptionally competent gene occur with myeloid differentiation and progress with differentiation. Additional histone modifications characteristic of active gene expression are acquired with stimulation. In each case, manipulation of these epigenetic variables altered the ability of the cell to express TNF-α. These studies demonstrate the importance of epigenetic regulation in the control of TNF-α expression. These findings may have relevance for inflammatory disorders in which TNF-α is overproduced.
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Topolyanskaya, S. V. "Tumor Necrosis Factor-Alpha and Age-Related Pathologies." Russian Archives of Internal Medicine 10, no. 6 (December 2, 2020): 414–21. http://dx.doi.org/10.20514/2226-6704-2020-10-6-414-421.
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Modern concepts about the «inflammaging» and the role of subclinical inflammation in various age-associated pathology are described in the review. Particular attention is paid to the tumor necrosis factor-α, a key cytokine that plays an important role in the pathogenesis of chronic inflammatory diseases as well as in aging. The increased levels of tumor necrosis factor-α leads to the onset and progression of various diseases, to severity of frailty, to disability and mortality of elderly persons. Tumor necrosis factor-α affects different risk factors for cardiovascular diseases, contributes to the onset and progression of atherosclerosis and related pathology. This cytokine can also aggravate various metabolic disorders, mainly — insulin resistance and diabetes mellitus. Tumor necrosis factor-α is a key cytokine that stimulates bone resorption (up to osteoporosis) and sarcopenia (up to cachexia). Currently available data confirm the important role of tumor necrosis factor-α in various age-associated disorders.
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Miao, Kun, Ling Zhou, Hongping Ba, Chenxi Li, Haiyan Gu, Bingjiao Yin, Jing Wang, Xiang-ping Yang, Zhuoya Li, and Dao Wen Wang. "Transmembrane tumor necrosis factor alpha attenuates pressure-overload cardiac hypertrophy via tumor necrosis factor receptor 2." PLOS Biology 18, no. 12 (December 3, 2020): e3000967. http://dx.doi.org/10.1371/journal.pbio.3000967.
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Tumor necrosis factor-alpha (TNF-α) plays an important pathogenic role in cardiac hypertrophy and heart failure (HF); however, anti-TNF is paradoxically negative in clinical trials and even worsens HF, indicating a possible protective role of TNF-α in HF. TNF-α exists in transmembrane (tmTNF-α) and soluble (sTNF-α) forms. Herein, we found that TNF receptor 1 (TNFR1) knockout (KO) or knockdown (KD) by short hairpin RNA or small interfering RNA (siRNA) significantly alleviated cardiac hypertrophy, heart dysfunction, fibrosis, and inflammation with increased tmTNF-α expression, whereas TNFR2 KO or KD exacerbated the pathological phenomena with increased sTNF-α secretion in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced cardiac hypertrophy in vivo and in vitro, respectively, indicating the beneficial effects of TNFR2 associated with tmTNF-α. Suppressing TNF-α converting enzyme by TNF-α Protease Inhibitor-1 (TAPI-1) to increase endogenous tmTNF-α expression significantly alleviated TAC-induced cardiac hypertrophy. Importantly, direct addition of exogenous tmTNF-α into cardiomyocytes in vitro significantly reduced ISO-induced cardiac hypertrophy and transcription of the pro-inflammatory cytokines and induced proliferation. The beneficial effects of tmTNF-α were completely blocked by TNFR2 KD in H9C2 cells and TNFR2 KO in primary myocardial cells. Furthermore, we demonstrated that tmTNF-α displayed antihypertrophic and anti-inflammatory effects by activating the AKT pathway and inhibiting the nuclear factor (NF)-κB pathway via TNFR2. Our data suggest that tmTNF-α exerts cardioprotective effects via TNFR2. Specific targeting of tmTNF-α processing, rather than anti-TNF therapy, may be more useful for the treatment of hypertrophy and HF.
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Cai, Weibo, Zachary J. Kerner, Hao Hong, and Jiangtao Sun. "Targeted Cancer Therapy with Tumor Necrosis Factor-Alpha." Biochemistry Insights 1 (January 2008): BCI.S901. http://dx.doi.org/10.4137/bci.s901.
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Tumor necrosis factor-alpha (TNF-α), a member of the TNF superfamily, was the first cytokine to be evaluated for cancer biotherapy. However, the clinical use of TNF-α is severely limited by its toxicity. Currently, TNF-α is administered only through locoregional drug delivery systems such as isolated limb perfusion and isolated hepatic perfusion. To reduce the systemic toxicity of TNF-α, various strategies have been explored over the last several decades. This review summarizes current state-of-the-art targeted cancer therapy using TNF-α. Passive targeting, cell-based therapy, gene therapy with inducible or tissue-specific promoters, targeted polymer-DNA complexes, tumor pre-targeting, antibody-TNF-α conjugate, scFv/TNF-α fusion proteins, and peptide/TNF-α fusion proteins have all been investigated to combat cancer. Many of these agents are already in advanced clinical trials. Molecular imaging, which can significantly speed up the drug development process, and nanomedicine, which can integrate both imaging and therapeutic components, has the potential to revolutionize future cancer patient management. Cooperative efforts from scientists within multiple disciplines, as well as close partnerships among many organizations/entities, are needed to quickly translate novel TNF-α-based therapeutics into clinical investigation.
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Suriano, April R., Amy N. Sanford, Nahmah Kim, Miae Oh, Sarah Kennedy, Mark J. Henderson, Kelly Dietzmann, and Kathleen E. Sullivan. "GCF2/LRRFIP1 Represses Tumor Necrosis Factor Alpha Expression." Molecular and Cellular Biology 25, no. 20 (October 15, 2005): 9073–81. http://dx.doi.org/10.1128/mcb.25.20.9073-9081.2005.
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ABSTRACT Tumor necrosis factor alpha (TNF-α) is an important mediator of inflammation, apoptosis, and the development of secondary lymphoid structures. Multiple polymorphic microsatellites have been identified in and around the gene, and there are also multiple single-base pair biallelic polymorphisms in the introns and promoter. The TNF-α −308 promoter polymorphism is a G-to-A transition which has been statistically associated with various autoimmune disorders. Some studies have found that it may directly mediate the increased transcription of TNF-α in some circumstances. This study characterizes proteins interacting at the polymorphic promoter site. Affinity purification of binding proteins and confirmatory chromatin immunoprecipitation assays were used to identify the proteins. Electrophoretic mobility shift analyses and surface plasmon resonance were used to define binding characteristics. Proteins interacting at this site include GCF2/LRRFIP1 and Ets-1. GCF2/LRRFIP1 appears to act as a repressor and occupies the −308 site in cells that do not make TNF-α. Cells competent to produce TNF-α have Ets-1 bound to the −308 promoter site. Active transcription is accompanied by NF-κB and c-Jun binding to the proximal promoter. Thus, dynamic changes on the TNF-α promoter, particularly at the −308 site, accompany the transition from repressed to active transcription. GCF2/LRRFIP1 is the first TNF-α repressor identified.
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Decourt, Boris, Debomoy K. Lahiri, and Marwan N. Sabbagh. "Targeting Tumor Necrosis Factor Alpha for Alzheimer’s Disease." Current Alzheimer Research 14, no. 4 (February 16, 2017): 412–25. http://dx.doi.org/10.2174/1567205013666160930110551.
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Alzheimer’s disease (AD) affects an estimated 44 million individuals worldwide, yet no therapeutic intervention is available to stop the progression of the dementia. Neuropathological hallmarks of AD are extracellular deposits of amyloid beta (Aβ) peptides assembled in plaques, intraneuronal accumulation of hyperphosphorylated tau protein forming tangles, and chronic inflammation. A pivotal molecule in inflammation is the pro-inflammatory cytokine TNF-α. Several lines of evidence using genetic and pharmacological manipulations indicate that TNF-α signaling exacerbates both Aβ and tau pathologies in vivo. Interestingly, preventive and intervention anti-inflammatory strategies demonstrated a reduction in brain pathology and an amelioration of cognitive function in rodent models of AD. Phase I and IIa clinical trials suggest that TNF-α inhibitors might slow down cognitive decline and improve daily activities in AD patients. In the present review, we summarize the evidence pointing towards a beneficial role of anti-TNF-α therapies to prevent or slow the progression of AD. We also present possible physical and pharmacological interventions to modulate TNF-α signaling in AD subjects along with their limitations.
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Tseng, Wei-Cheng, Hou-Chuan Lai, Yi-Hsuan Huang, Shun-Ming Chan, and Zhi-Fu Wu. "Tumor Necrosis Factor Alpha: Implications of Anesthesia on Cancers." Cancers 15, no. 3 (January 25, 2023): 739. http://dx.doi.org/10.3390/cancers15030739.
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Cancer remains a major public health issue and a leading cause of death worldwide. Despite advancements in chemotherapy, radiation therapy, and immunotherapy, surgery is the mainstay of cancer treatment for solid tumors. However, tumor cells are known to disseminate into the vascular and lymphatic systems during surgical manipulation. Additionally, surgery-induced stress responses can produce an immunosuppressive environment that is favorable for cancer relapse. Up to 90% of cancer-related deaths are the result of metastatic disease after surgical resection. Emerging evidence shows that the interactions between tumor cells and the tumor microenvironment (TME) not only play decisive roles in tumor initiation, progression, and metastasis but also have profound effects on therapeutic efficacy. Tumor necrosis factor alpha (TNF-α), a pleiotropic cytokine contributing to both physiological and pathological processes, is one of the main mediators of inflammation-associated carcinogenesis in the TME. Because TNF-α signaling may modulate the course of cancer, it can be therapeutically targeted to ameliorate clinical outcomes. As the incidence of cancer continues to grow, approximately 80% of cancer patients require anesthesia during cancer care for diagnostic, therapeutic, or palliative procedures, and over 60% of cancer patients receive anesthesia for primary surgical resection. Numerous studies have demonstrated that perioperative management, including surgical manipulation, anesthetics/analgesics, and other supportive care, may alter the TME and cancer progression by affecting inflammatory or immune responses during cancer surgery, but the literature about the impact of anesthesia on the TNF-α production and cancer progression is limited. Therefore, this review summarizes the current knowledge of the implications of anesthesia on cancers from the insights of TNF-α release and provides future anesthetic strategies for improving oncological survival.
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Gürsel, G., N. Gökçora, Ş. Elbeg, B. Samurkaşoğlu, and N. Ekim. "Tumor necrosis factor-alpha (TNF-α) in pleural fluids." Tubercle and Lung Disease 76, no. 4 (August 1995): 370–71. http://dx.doi.org/10.1016/s0962-8479(05)80039-5.
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Sutanto, Felix Candra, Max F. J. Mantik, and Vivekenanda Pateda. "Hubungan antara Tumor Necrosis Factor Alpha dengan Demam Berdarah Dengue." Sari Pediatri 15, no. 4 (November 10, 2016): 244. http://dx.doi.org/10.14238/sp15.4.2013.244-8.
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Latar belakang. Sampai saat ini patogenesis demam berdarah dengue (DBD) belum dipahami secara sempurna. Pada kasus DBD didapatkan adanya peningkatan kadar TNF-α, sitokin yang poten dalam meningkatkan permeabilitas pembuluh darah. Penelitian sebelumnya mendapatkan adanya peningkatan kadar TNF-α yang bermakna pada DBD.Tujuan. Mengetahui hubungan antara kadar TNF-α dengan keparahan DBD.Metode. Penelitian analitik observasional dengan pendekatan potong lintang selama bulan Ju li hingga Desember 2011. Pasien didiagnosis DBD berdasarkan kriteria WHO. Data berupa hemoglobin, hematokrit, jumlah leukosit, jumlah trombosit, dan kadar TNF-α dikumpulkan selama penelitian. Analisis statistik menggunakan korelasi Spearman’s Rho dengan tingkat kemaknaan p<0,05.Hasil. Didapatkan tiga puluh delapan anak, 27 di antaranya didiagnosis DBD tanpa syok dan 11 DBD dengan syok. Rerata usia kelompok DBD tanpa syok adalah 7,56 (SB 3,06) tahun (95% IK 6,35-8,76 tahun) dan rerata usia kelompok DBD dengan syok adalah 6,82 (SB 3,25) tahun (95% IK 4,63-9,00 tahun). Rerata kadar TNF-α kelompok DBD tanpa syok adalah 13,13 (SB 7,57) pg/ml (95% IK 10,14-16,13 pg/ml) dan rerata kadar TNF-α kelompok DBD dengan syok adalah 260,52 (SB 239,08) pg/ml (95% IK 99,90-421,13 pg/ml). Didapatkan hubungan positif yang bermakna antara kadar TNFα plasma dengan tingkat keparahan/derajat DBD (rs 0,885; p<0,001).Kesimpulan. Semakin berat derajat DBD yang terjadi semakin tinggi kadar TNF-α
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Sutanto, Felix Candra, Max F. J. Mantik, and Vivekenanda Pateda. "Hubungan antara Tumor Necrosis Factor Alpha dengan Demam Berdarah Dengue." Sari Pediatri 15, no. 4 (November 10, 2016): 244. http://dx.doi.org/10.14238/sp15.4.2013.244-8.
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Latar belakang. Sampai saat ini patogenesis demam berdarah dengue (DBD) belum dipahami secara sempurna. Pada kasus DBD didapatkan adanya peningkatan kadar TNF-α, sitokin yang poten dalam meningkatkan permeabilitas pembuluh darah. Penelitian sebelumnya mendapatkan adanya peningkatan kadar TNF-α yang bermakna pada DBD.Tujuan. Mengetahui hubungan antara kadar TNF-α dengan keparahan DBD.Metode. Penelitian analitik observasional dengan pendekatan potong lintang selama bulan Ju li hingga Desember 2011. Pasien didiagnosis DBD berdasarkan kriteria WHO. Data berupa hemoglobin, hematokrit, jumlah leukosit, jumlah trombosit, dan kadar TNF-α dikumpulkan selama penelitian. Analisis statistik menggunakan korelasi Spearman’s Rho dengan tingkat kemaknaan p<0,05.Hasil. Didapatkan tiga puluh delapan anak, 27 di antaranya didiagnosis DBD tanpa syok dan 11 DBD dengan syok. Rerata usia kelompok DBD tanpa syok adalah 7,56 (SB 3,06) tahun (95% IK 6,35-8,76 tahun) dan rerata usia kelompok DBD dengan syok adalah 6,82 (SB 3,25) tahun (95% IK 4,63-9,00 tahun). Rerata kadar TNF-α kelompok DBD tanpa syok adalah 13,13 (SB 7,57) pg/ml (95% IK 10,14-16,13 pg/ml) dan rerata kadar TNF-α kelompok DBD dengan syok adalah 260,52 (SB 239,08) pg/ml (95% IK 99,90-421,13 pg/ml). Didapatkan hubungan positif yang bermakna antara kadar TNFα plasma dengan tingkat keparahan/derajat DBD (rs 0,885; p<0,001).Kesimpulan. Semakin berat derajat DBD yang terjadi semakin tinggi kadar TNF-α
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Chen, Huacong, Hua Xu, Jiali Dong, Jing Li, and Fayez K. Ghishan. "Tumor necrosis factor-alpha impairs intestinal phosphate absorption in colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 4 (April 2009): G775—G781. http://dx.doi.org/10.1152/ajpgi.90722.2008.
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Phosphate homeostasis is critical for many physiological functions. Up to 85% of phosphate is stored in bone and teeth. The remaining 15% is distributed in cells. Phosphate absorption across the brush-border membrane (BBM) of enterocytes occurs mainly via a sodium-dependent pathway, which is mediated by type IIb sodium-phosphate cotransporters (NaPi-IIb). Patients of inflammatory bowel diseases (IBDs) suffer not only from diarrhea and nutrient malabsorption but also from bone loss. About 31–59% of patients with IBD develop bone disorders. Since the intestine is a primary location for dietary phosphate absorption, it is logical to postulate that there is an inverse relationship between gastrointestinal disorders and phosphate transport, which, in turn, contributes to bone disorders observed in patients with IBD. Phosphate absorption and NaPi-IIb expression was studied with BBM vesicles isolated from trinitrobenzene sulphonic acid (TNBS) animals as well as in Caco-2 cells. The mechanism of TNF-α downregulation of NaPi-IIb expression was investigated by luciferase assay, gel mobility shift assay (GMSA), and coimmunoprecipitation. Intestinal phosphate absorption mediated by NaPi-IIb was reduced both in TNBS colitis and in TNF-α-treated cells. Transient transfection indicated that TNF-α inhibits NaPi-IIb expression by reducing NaPi-IIb basal promoter activity. GMSAs identified NF1 protein as an important factor in TNF-α-mediated NaPi-IIb downregulation. Signaling transduction study and coimmunoprecipitation suggested that TNF-α interacts with EGF receptor to activate ERK1/2 pathway. Intestinal phosphate absorption mediated by NaPi-IIb protein is reduced in colitis. This inhibition is mediated by the proinflammatory cytokine TNF-α through a novel molecular mechanism involving TNF-α/EGF receptor interaction.
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Joo, Hee Kyoung, Sae Cheol Oh, Eun Jung Cho, Kyoung Sook Park, Ji Young Lee, Eun Ji Lee, Sang Ki Lee, Hyo Shin Kim, Jin Bong Park, and Byeong Hwa Jeon. "Midazolam Inhibits Tumor Necrosis Factor-α–induced Endothelial Activation." Anesthesiology 110, no. 1 (January 1, 2009): 106–12. http://dx.doi.org/10.1097/aln.0b013e318190bc69.
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Background Midazolam is widely used as an intravenous sedative. However, the role of midazolam on vascular endothelial activation is still unknown. The present study explores the action of midazolam on endothelial activation and its role to peripheral benzodiazepine receptor (PBR) in cultured human umbilical vein endothelial cells. Methods Intracellular localization of PBR in human umbilical vein endothelial cells was visualized with immunofluorescent staining. Monocyte adhesion and vascular cell adhesion molecule-1 expression were measured with monocyte adhesion assay and Western blot analysis. Involvement of PBR was assessed by using specific antagonists and small interfering RNA against PBR. Results PBR was localized in the mitochondria of human umbilical vein endothelial cells. Midazolam significantly inhibited tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 and monocyte adhesion in a dose-dependent manner (1-30 microM). The midazolam-mediated suppression on the tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression and monocyte adhesion were inhibited by the pretreatment of PK11195 and not inhibited by the flumazenil. Transfection of small interfering RNA for PBR decreased the expression of PBR (18 kDa) in human umbilical vein endothelial cells. Midazolam-mediated suppression on the tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 expression was abrogated by the transfection of small interfering RNA for PBR. Conclusion These results suggest that midazolam has an inhibitory action on the endothelial activation and that its action is related to the activation of peripheral benzodiazepine receptor localized in mitochondria of the endothelial cells.
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Papasian, Christopher J., Richard Silverstein, Jian Jun Gao, David M. Bamberger, and David C. Morrison. "Anomalous Role of Tumor Necrosis Factor Alpha in Experimental Enterococcal Infection." Infection and Immunity 70, no. 12 (December 2002): 6628–37. http://dx.doi.org/10.1128/iai.70.12.6628-6637.2002.
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ABSTRACT The murine d-galactosamine (d-gal) model of tumor necrosis factor alpha (TNF-α) hypersensitization was used as an initial tool to investigate the potential contribution of TNF-α to lethal intraperitoneal (i.p.) infection with Enterococcus faecalis. d-gal sensitized mice to lethal E. faecalis infection, whereas dexamethasone and neutralizing anti-TNF-α antibody protected d-gal-treated, E. faecalis-infected mice, implicating TNF-α in the lethal response to E. faecalis infection in d-gal-treated mice. Circulating TNF-α was undetectable for at least 8 h following i.p. E. faecalis infection, although low peritoneal levels of TNF-α were detected within 3 h, suggesting that localized TNF-α production contributed to the lethal response to E. faecalis infection in d-gal-treated mice. Although i.p. E. faecalis infection failed to induce a detectable systemic TNF-α response, circulating Interleukin-6 (IL-6) was detected within 3 h of infection. IL-6 was also detected in the peritoneum within an hour of infection, prior to the appearance of peritoneal TNF-α. In striking contrast to in vivo results, E. faecalis induced a potent and rapid TNF-α response from both mouse peritoneal macrophages and the RAW 264.7 cell line in vitro. This led us to hypothesize that TNF-α production in response to E. faecalis infection is suppressed by IL-6 in vivo. In vitro experiments demonstrated a statistically significant, but modest, inhibitory effect of IL-6 on TNF-α production by RAW cells stimulated with E. faecalis. Collectively, these data indicate that acute, lethal E. faecalis infection appears to induce an unusual cytokine response that differs in character from that previously described for most other gram-positive and gram-negative bacteria.
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Gandini, Andi Lis Arming, Joko Sapto Pramono, Umi Kalsum, Supriadi Supriadi, and Azhari Azhari. "Effectiveness of Asthma Gymnastic on Levels of Tumor Necrosis Factor Alpha (TNF-α) in Asthma Patients." Health Notions 4, no. 7 (July 26, 2020): 205–10. http://dx.doi.org/10.33846/hn40702.
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Asthma is a chronic inflammation of the airways that involves many cells and their elements. Non-pharmacological treatment of Asthma, one of them is Asthma Gymnastics. The purpose of this study was to determine the effect of asthma exercises on levels of Tumor Necrosis Factor Alpha (TNF-α) in asthma patients.
This study used a quasi-experiment method of pre and post-test with control. The sample size of the intervention group was 8 people and the control group was 7 people. The results of hypothesis testing with the Wilcoxon Test found that there was an influence of asthma gymnastic intervention on the levels of Tumor Necrosis Factor Alpha (TNF-α) with a p-value of 0.046. The result of this study showed the effect of asthma exercises on levels of Tumor Necrosis Factor Alpha (TNF-α) in asthma patients. For further research, it is expected to research by increasing the number of treatments in the intervention group and controlling the drugs taken so that it is more optimal in its effect on respondents.
Keywords: asthma; Tumor Necrosis Factor alpha (TNF-α); asthma gymnastics
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Matsuzaki, Hidenori, Hiroshi Kobayashi, Tatsuo Yagyu, Kiyoshi Wakahara, Toshiharu Kondo, Noriyuki Kurita, Hideo Sekino, et al. "Bikunin Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Induction in Macrophages." Clinical Diagnostic Laboratory Immunology 11, no. 6 (November 2004): 1140–47. http://dx.doi.org/10.1128/cdli.11.6.1140-1147.2004.
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ABSTRACT Bikunin, a Kunitz-type protease inhibitor, exhibits anti-inflammatory activity in protection against cancer and inflammation. To investigate the molecular mechanism of this inhibition, we analyzed the effect of bikunin on tumor necrosis factor alpha (TNF-α) production in human peripheral mononuclear cells stimulated by lipopolysaccharide (LPS), an inflammatory inducer. Here, we show the following results. (i) LPS induced TNF-α expression in time- and dose-dependent manners through phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase pathways. (ii) Bikunin inhibits LPS-induced up-regulation of TNF-α protein expression in a dose-dependent manner, reaching 60% inhibition at the highest doses of bikunin tested (5.0 μM). (iii) Inhibition by bikunin of TNF-α induction correlates with the suppressive capacity of ERK1/2, JNK, and p38 signaling pathways, implicating repressions of at least three different signals in the inhibition. (iv) Bikunin blocks the induction of TNF-α target molecules interleukin-1β (IL-1β) and IL-6 proteins. (v) Bikunin is functional in vivo, and this glycoprotein blocks systemic TNF-α release in mice challenged with LPS. (vi) Finally, bikunin can prevent LPS-induced lethality. In conclusion, bikunin significantly inhibits LPS-induced TNF-α production, suggesting a mechanism of anti-inflammation by bikunin through control of cytokine induction during inflammation. Bikunin might be a candidate for the treatment of inflammation, including septic shock.
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Efffendy, Elmeida, Mustafa Mahmud Amin, and Nurul Utami. "Role of Tumor Necrosis Factor-Alpha in Schizophrenia and Cognitive Impairment." Open Access Macedonian Journal of Medical Sciences 9, T3 (May 20, 2021): 160–63. http://dx.doi.org/10.3889/oamjms.2021.6289.
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Background: Neuroinflammation and excitotoxicity play a key role as triggers and support for neurodegenerative processes, increase levels of TNF-α have been found in schizophrenic patients. Improved inflammatory processes have been demonstrated in acute and chronic schizophrenia. In schizophrenia is characterized by a collection of core symptoms that trigger individuals experiencing several cognitive disorders.
Objective: To investigate the relationship of serum TNF-α levels to impaired cognitive function in schizophrenic patients in Medan, Indonesia.
Method: This research is cross sectional analytical correlative study involving 40 male schizophrenic patients at Prof. Dr. M. Ildrem Mental Hospital through July to September 2019 that fulfilled our inclusion and exclusion criteria. Serum TNF-α levels were analyzed using Quantikine HS Human TNF-α Assay with a minimum detection limit of 0.1062 pg/ml while in the other hand, cognitive function test was carried out by using the Mini Mental State Examination.
Results: Serum TNF-α levels with a mean of 25.1216 with a standard deviation of 1.7629. There is a positive correlation with moderate correlation (r = 0.4 - <0.6) on cognitive function with the strength of correlation r = 0.434
Conclusion: We found that there is a link between serum TNF-α level and cognitive function as assessed with the Mini-Mental State Examination (MMSE).
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Shrestha, Sajeev, Manisha Neupane, Shivalal Sharma, and Madhab Lamsal. "Assessment of tumor necrosis factor- alpha in gingivitis and periodontitis patients." International Journal of Dental Research 5, no. 2 (June 29, 2017): 108. http://dx.doi.org/10.14419/ijdr.v5i2.7874.
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Background: Tumor necrosis factor-α, one of the cytokines, is released in various chronic inflammatory diseases including periodontitis.Aims: To estimate the level of Tumor necrosis factor- alpha (TNF-α) in gingivitis and periodontitis patientsSettings and Design: A cross-sectional study was conducted. A total of 75 patients were recruited by purposive sampling technique among the patients visiting the Department of Periodontology and Oral Implantology during the period one year from August 2014 to July 2015.Material and methods: The recruited samples were divided into gingivitis and periodontitis groups based on clinical attachment level (CAL). A periodontitis subject was defined as having at least 4 sites with pocket depth (PD) >3mm and at least 4 sites with CAL>3 mm, while gingivitis group included the subjects having no CAL measurements greater than 3 mm with signs of inflammation. The TNF-α level was measured using the RayBio Human TNF-alpha ELISA (Enzyme-linked Immunosorbent Assay) kit.Results: The Median TNF-α interquartile range (IQR) (minimum-maximum) in gingivitis and periodontitis was 58.37 (32.63 – 198.77) and 111.89 (39.27 – 215.0) pg/ml, respectively.Conclusion: The level of TNF-α was found to be higher in periodontitis group compared to gingivitis group, although the result was not statistically significant.
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Morrison, Thomas E., Amy Mauser, Aloysius Klingelhutz, and Shannon C. Kenney. "Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1." Journal of Virology 78, no. 1 (January 1, 2004): 544–49. http://dx.doi.org/10.1128/jvi.78.1.544-549.2004.
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ABSTRACT Tumor necrosis factor alpha (TNF-α) is a key mediator of host immune and inflammatory responses and inhibits herpesvirus replication by cytolytic and noncytolytic mechanisms. TNF-α effects are primarily mediated through the major TNF-α receptor, TNF-R1, which is constitutively expressed in most cell types. Here we show that the Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-α activation of target genes and TNF-α-induced cell death. These effects are mediated by down-regulation of the promoter for TNF-R1. Additionally, we demonstrate that expression of TNF-R1 is downregulated during the EBV lytic replication cycle. Thus, EBV has developed a novel mechanism for evading TNF-α antiviral effects during lytic reactivation or primary infection.
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Thalmaier, Ulrike, Norbert Lehn, Klaus Pfeffer, Manfred Stolte, Michael Vieth, and Wulf Schneider-Brachert. "Role of Tumor Necrosis Factor Alpha in Helicobacter pylori Gastritis in Tumor Necrosis Factor Receptor 1-Deficient Mice." Infection and Immunity 70, no. 6 (June 2002): 3149–55. http://dx.doi.org/10.1128/iai.70.6.3149-3155.2002.
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ABSTRACT Increased gastric production of interleukin 8 and tumor necrosis factor alpha (TNF-α) has been implicated in the pathogenesis of Helicobacter pylori-associated gastroduodenal disease. In the present study we used a mouse model to demonstrate whether loss of the tumor necrosis factor receptor 1 (TNF-R1) function leads to differences in gastric inflammation or the systemic immune response in H. pylori infection. Six different clinical isolates of H. pylori (three cytotoxin-positive and three cytotoxin-negative strains) were adapted to C57BL/6 mice. TNF-R1-deficient (TNF-R1−/−) mice (n = 19) and isogenetic controls (n = 24) were infected and sacrificed after 4 weeks of infection. Inflammation of the stomach and the humoral immune response to H. pylori were evaluated by histological, immunohistochemical, and serological methods. There was no detectable difference in the grade or activity of gastritis in TNF-R1−/− mice when they were compared with wild-type mice, but the number of lymphoid aggregates was slightly reduced in the gastric mucosa of TNF-R1−/− mice. Interestingly, total immunoglobulin G (IgG), as well as IgG1, IgG2b, and IgG3, H. pylori-specific antibody titers were significantly higher in wild-type mice. As revealed by immunoblot analysis, the difference in reactivity against H. pylori antigens was not based on a failure to recognize single H. pylori antigens in TNF-R1−/− mice. We therefore suggest that TNF-R1-mediated TNF-α signals might support a systemic humoral immune response against H. pylori and that the gastric inflammatory response to H. pylori infection seems to be independent of TNF-R1-mediated signals.
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Mężyk-Kopeć, Renata, Małgorzata Bzowska, Jan Potempa, Monika Bzowska, Natalia Jura, Aneta Sroka, Roy A. Black, and Joanna Bereta. "Inactivation of Membrane Tumor Necrosis Factor Alpha by Gingipains from Porphyromonas gingivalis." Infection and Immunity 73, no. 3 (March 2005): 1506–14. http://dx.doi.org/10.1128/iai.73.3.1506-1514.2005.
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ABSTRACT Gingipains are cysteine proteinases produced by Porphyromonas gingivalis, a major causative bacterium of adult periodontitis. They consist of arginine-specific (HRgpA and RgpB) and lysine-specific (Kgp) proteinases. Gingipains strongly affect the host defense system by degrading some cytokines, components of the complement system, and several immune cell receptors. In an in vitro model, gingipains were shown to degrade soluble tumor necrosis factor alpha (TNF-α). However, since membrane TNF-α shows strong biological activity, especially in local inflammatory lesions, it was worth investigating whether gingipains might also destroy membrane TNF-α and limit its biological activities. To avoid a possible influence of gingipains on ADAM17, the secretase of TNF-α, the majority of experiments were performed using ADAM17−/− fibroblasts stably transfected with cDNA of human pro-TNF-α (ADAM17−/− TNF+). Arginine-specific gingipains (Rgp's) strongly diminished the level of TNF-α on the cell surface as measured by flow cytometry, and this process was not accompanied by an increased concentration of soluble TNF-α in the culture medium. Degradation of membrane TNF-α by Rgp's correlated with a strong decrease in TNF-α-mediated biological activities of ADAM17−/− TNF+ cells. First, the activation state of transcription factor NF-κB was suppressed; second, the cells were no longer able to induce apoptosis in HL-60 cells. Kgp was also able to cleave membrane TNF-α, but its effect was much weaker than that of Rgp's. Gingipains also limited the binding of native TNF-α to the target cells. Thus, gingipains are able not only to cleave soluble TNF-α but also to destroy the membrane form of the cytokine, which may additionally dysregulate the cytokine network.
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Xue, Yimeng, Xianwei Zeng, Wen-Jun Tu, and Jizong Zhao. "Tumor Necrosis Factor-α: The Next Marker of Stroke." Disease Markers 2022 (February 27, 2022): 1–8. http://dx.doi.org/10.1155/2022/2395269.
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Although there is no shortage of research on the markers for stroke, to our knowledge, there are no clear markers that can meet the needs of clinical prediction and treatment. The inflammatory cascade is a critical process that persists and functions throughout the stroke process, ultimately worsening stroke outcomes and increasing mortality. Numerous inflammatory factors, including tumor necrosis factor (TNF), are involved in this process. These inflammatory factors play a dual role during stroke, and their mechanisms are complex. As one of the representatives, TNF is the primary regulator of the immune system and plays an essential role in the spread of inflammation. In researches done over the last few years, tumor necrosis factor-alpha (TNF-α) has emerged as a potential marker for stroke because of its essential role in stroke. This review summarizes the latest research on TNF-α in stroke and explores its potential as a therapeutic target.
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Ogata, Masanori, Takashi Matsui, Toshiro Kita, and Akio Shigematsu. "Carrageenan Primes Leukocytes To Enhance Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Production." Infection and Immunity 67, no. 7 (July 1, 1999): 3284–89. http://dx.doi.org/10.1128/iai.67.7.3284-3289.1999.
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ABSTRACT We have previously reported that pretreatment with carrageenan (CAR) enhances lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-α) production in and lethality for mice. Whole blood cultured in vitro was used to show that CAR pretreatment results in about a 200-fold increase in LPS-induced TNF-α production. CAR by itself did not induce TNF-α production. However, CAR-treated cultured medium sensitized whole blood to make more LPS-induced TNF than did saline-treated cultured medium in vitro. It was also demonstrated that CAR pretreatment increases TNF-α mRNA levels of both blood cells and peritoneal exudate cells, but not of bone marrow cells. Immunoelectron microscopic analysis revealed that polymorphonuclear leukocytes and macrophages are TNF-α-producing cells in CAR-treated mice. In CAR-treated mice, TNF-α was seen early after LPS injection in leukocytes in hepatic sinusoids and on the surfaces of endothelial cells. TNF-α was also detected late after LPS injection in hepatocytes which become edematous. These results suggest that CAR primes leukocytes to produce TNF-α in response to LPS and that they play an important role in the pathogenesis of liver injury.
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Perez, Denise, and Eileen White. "E1A Sensitizes Cells to Tumor Necrosis Factor Alpha by Downregulating c-FLIPS." Journal of Virology 77, no. 4 (February 15, 2003): 2651–62. http://dx.doi.org/10.1128/jvi.77.4.2651-2662.2003.
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ABSTRACT Tumor necrosis factor alpha (TNF-α) activates both apoptosis and NF-κB-dependent survival pathways, the former of which requires inhibition of gene expression to be manifested. c-FLIP is a TNF-α-induced gene that inhibits caspase-8 activation during TNF-α signaling. Adenovirus infection and E1A expression sensitize cells to TNF-α by allowing apoptosis in the absence of inhibitors of gene expression, suggesting that it may be disabling a survival signaling pathway. E1A promoted TNF-α-mediated activation of caspase-8, suggesting that sensitivity was occurring at the level of the death-inducing signaling complex. Furthermore, E1A expression downregulated c-FLIPS expression and prevented its induction by TNF-α. c-FLIPS and viral FLIP expression rescued E1A-mediated sensitization to TNF-α by restoring the resistance of caspase-8 to activation, thereby preventing cell death. E1A inhibited TNF-α-dependent induction of c-FLIPS mRNA and stimulated ubiquitination- and proteasome-dependent degradation of c-FLIPS protein. Since elevated c-FLIP levels confer resistance to apoptosis and promote tumorigenicity, interference with its induction by NF-κB and stimulation of its destruction in the proteasome may provide novel therapeutic approaches for facilitating the elimination of apoptosis-refractory tumor cells.
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Ali, M. S., Salwa H. Al-Rubaei, and Najwa S. Ahmed. "Tumor necrosis factor alpha as a potential marker for prostate cancer." Journal of Biotechnology Research Center 14, no. 1 (January 1, 2020): 5–9. http://dx.doi.org/10.24126/jobrc.2020.14.1.582.
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Background: Prostate cancer is currently the most common cause of cancer death in men. The exact cause of developing prostate cancer is not known though inflammation, ageing, ethnicity and heredity are important factors involved in the initiation and development of this cancer.
Aim of study : The aim of this study to determine the levels of prostate specific antigen (PSA), tumor necrosis factor alpha (TNF-α), testosterone (T) and dihydrotestosterone (DHT) in sera of thirty patients with prostate cancer (PCa), thirty patients with benign prostate hyperplasia (BPH) and in thirty health volunteers, T/DHT ratio was also calculated.
Result: There was a significant increase in the levels of PSA, TNF-α, T and T/DHT ratio in PCa as well as BPH patients compared to the controls. There was a significant decrease in DHT levels in both PCa and BPH compared to the controls.
Conclusion: TNF-α could serve as a potential marker for the diagnosis of PCa.
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Olmos, Gabriel, and Jerònia Lladó. "Tumor Necrosis Factor Alpha: A Link between Neuroinflammation and Excitotoxicity." Mediators of Inflammation 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/861231.
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Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine that exerts both homeostatic and pathophysiological roles in the central nervous system. In pathological conditions, microglia release large amounts of TNF-α; thisde novoproduction of TNF-αis an important component of the so-called neuroinflammatory response that is associated with several neurological disorders. In addition, TNF-αcan potentiate glutamate-mediated cytotoxicity by two complementary mechanisms: indirectly, by inhibiting glutamate transport on astrocytes, and directly, by rapidly triggering the surface expression of Ca+2permeable-AMPA receptors and NMDA receptors, while decreasing inhibitory GABAAreceptors on neurons. Thus, the net effect of TNF-αis to alter the balance of excitation and inhibition resulting in a higher synaptic excitatory/inhibitory ratio. This review summarizes the current knowledge of the cellular and molecular mechanisms by which TNF-αlinks the neuroinflammatory and excitotoxic processes that occur in several neurodegenerative diseases, but with a special emphasis on amyotrophic lateral sclerosis (ALS). As microglial activation and upregulation of TNF-αexpression is a common feature of several CNS diseases, as well as chronic opioid exposure and neuropathic pain, modulating TNF-αsignaling may represent a valuable target for intervention.
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Madigan, Michele C., Alfredo A. Sadun, Nina S. Rao, Pravin U. Dugel, Wendy N. Tenhula, and Parkash S. Gill. "Tumor necrosis factor-alpha (TNF-α)-induced optic neuropathy in rabbits." Neurological Research 18, no. 2 (April 1996): 176–84. http://dx.doi.org/10.1080/01616412.1996.11740399.
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Serin, Ýbrahim Serdar, Bülent Özçelik, Mustafa Bapbu∂, Hüseyin Kýlýç, Derya Okur, and Rusen Erez. "Predictive value of tumor necrosis factor alpha (TNF-α) in preeclampsia." European Journal of Obstetrics & Gynecology and Reproductive Biology 100, no. 2 (January 2002): 143–45. http://dx.doi.org/10.1016/s0301-2115(01)00484-5.
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Olejnik, Alicja K., and Ewa Brzezińska-Błaszczyk. "Tumor necrosis factor alpha (TNF-α) modulates rat mast cell reactivity." Immunology Letters 64, no. 2-3 (December 1998): 167–71. http://dx.doi.org/10.1016/s0165-2478(98)00106-0.
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Sundararajan, Ramya, and Eileen White. "E1B 19K Blocks Bax Oligomerization and Tumor Necrosis Factor Alpha-Mediated Apoptosis." Journal of Virology 75, no. 16 (August 15, 2001): 7506–16. http://dx.doi.org/10.1128/jvi.75.16.7506-7516.2001.
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ABSTRACT Tumor necrosis factor alpha (TNF-α)-mediated death signaling causes the recruitment of monomeric pro- apoptotic Bax into a 500-kDa protein complex. The adenovirus Bcl-2 homologue, E1B 19K, inhibits TNF-α-mediated apoptosis, interacts with Bax, and blocked the formation of the 500-kDa Bax complex. TNF-α and truncated Bid induced Bax-Bax cross-linking, indicative of oligomerization, and E1B 19K expression during infection inhibited this TNF-α-mediated Bax oligomerization. TNF-α signaled conformation changes at the Bax amino and carboxy termini. Exposure of the Bax amino terminus facilitates E1B 19K-Bax binding, which prevented exposure of the carboxy-terminal Bax Bcl-2 homology region 2 epitope. Inhibition of Bax oligomerization by E1B 19K is an activity that bears striking similarity to the means by which bacterial immunity proteins block pore formation by bacterial toxins which have structural homology to Bax.
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Seo, Sang Heui, and Robert G. Webster. "Tumor Necrosis Factor Alpha Exerts Powerful Anti-Influenza Virus Effects in Lung Epithelial Cells." Journal of Virology 76, no. 3 (February 1, 2002): 1071–76. http://dx.doi.org/10.1128/jvi.76.3.1071-1076.2002.
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ABSTRACT Previous studies have associated influenza virus-induced expression of inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), with influenza pathogenesis in the human respiratory tract and have suggested that alpha and beta interferons are the first cytokines recruited to counteract such infection. However, we report here that TNF-α has powerful anti-influenza virus activity. When infected with influenza virus, cultured porcine lung epithelial cells expressed TNF-α in a dose-dependent manner. Expression of TNF-α was induced only by replicating virus. TNF-α showed strong antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF-α was greater than that of gamma or alpha interferon. These findings suggest that TNF-α serves as the first line of defense against influenza virus infection in the natural host.
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Lin, Ruei-Lung, Yu-Jung Lin, Marcus J. Geer, Richard Kryscio, and Lu-Yuan Lee. "Pulmonary chemoreflex responses are potentiated by tumor necrosis factor-alpha in mice." Journal of Applied Physiology 114, no. 11 (June 1, 2013): 1536–43. http://dx.doi.org/10.1152/japplphysiol.01301.2012.
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Inhalation of tumor necrosis factor-alpha (TNF-α), a proinflammatory cytokine, induces airway hyperresponsiveness, and the underlying mechanism is not fully understood. Hypersensitivity of vagal bronchopulmonary C-fiber afferents is known to contribute to the airway hyperresponsiveness during an airway inflammatory reaction. Because activation of these afferents can elicit pulmonary chemoreflexes, this study was designed to determine if a pretreatment with TNF-α induced airway inflammation and enhanced the pulmonary chemoreflex sensitivity in anesthetized mice; and if so, whether the effect was mediated through activation of either or both of the TNF receptors, p55 and p75. Our results showed that TNF-α instilled into the lung caused an increased sensitivity of pulmonary chemoreflex responses to various chemical stimulants of the vagal bronchopulmonary C-fiber afferents. The increased sensitivity was found 24 h later, persisted at 48 h, and then gradually declined after several days. The TNF-α-induced airway hypersensitivity was accompanied by airway inflammation as shown by a striking elevation of the levels of eosinophils and neutrophils, several potent bronchoactive inflammatory mediators, and proinflammatory cytokines in the bronchoalveolar lavage fluid. Furthermore, the increase in pulmonary chemoreflex response caused by TNF-α was partially abrogated in both p55-null and p75-null mice, but completely abolished in p55/p75-null mice. In conclusion, TNF-α pretreatment induced airway inflammation and a sustained elevation of pulmonary chemoreflex sensitivity, which was mediated through an activation of both types of TNF receptors.
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Collins, Rachel A., and Miranda D. Grounds. "The Role of Tumor Necrosis Factor-alpha (TNF-α) in Skeletal Muscle Regeneration." Journal of Histochemistry & Cytochemistry 49, no. 8 (August 2001): 989–1001. http://dx.doi.org/10.1177/002215540104900807.
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The role of tumor necrosis factor-alpha (TNF-α), an important mediator of the inflammatory response after injury, was investigated in regenerating skeletal muscle. The pattern of expression of TNF-α during muscle regeneration was examined by immunohistochemistry in tissue sections of crush-injured or transplanted muscle autografts and in primary cultures of adult skeletal muscle. TNF-α was highly expressed in injured myofibers, inflammatory cells, endothelial cells, fibroblasts, and mast cells. Myoblasts and myotubes also expressed TNF-α in primary muscle cultures and tissue sections. The essential role of TNF-α and its homologue lymphotoxin-alpha (LT-α) during muscle regeneration was assessed by basic histology in TNF-α(–) and TNF-α(-/-)/LT-α(-/-) mice. No difference was apparent in the onset or pattern of muscle regeneration (i.e., inflammatory response, activation and fusion of myoblasts) between the two strains of null mice or between nulls and normal control mice. However, both strains of null mice appeared more prone to bystander damage of host muscle and regeneration distant from the site of injury/transplantation. Although expression of TNF-α may play an important role in muscle regeneration, the studies in the null mice show that redundancy within the cytokine system (or some other response) can effectively compensate for the absence of TNF-α in vivo. (J Histochem Cytochem 49:989–1001, 2001)
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Sysoeva, G. M., E. I. Ryabchikova, O. V. Simakova, E. A. Volosnikova, L. R. Lebedev, and E. D. Danilenko. "EVALUATION OF ANTITUMOR ACTIVITY OF TUMOR NECROSIS FACTOR ALPHA WITHIN THE ARTIFICIAL VIRUS-LIKE PARTICLE." Russian Journal of Biotherapy 19, no. 1 (March 22, 2020): 96–103. http://dx.doi.org/10.17650/1726-9784-2019-19-1-96-103.
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Introduction. Tumor necrosis factor α (TNF-α) is a natural cytokine, characterized by pronounced antitumor properties. A wide range of side effects serves as an obstacle for the use of TNF-α in clinical practice. One of the ways to improve its therapeutic properties is to increase the tropism of the cytokine to the tumor tissue by incorporating it into the targeted delivery system.The aim of the study was to evaluate the antitumor activity of the preparation containing TNF-α as part of the artificial “virus-like particle” (VLP-TNF-α), developed in SRC VB “Vector” as a transport system for delivering proteins to target cells.Materials and methods. The antitumor effect of VLP-TNF-α preparation was evaluated in experimental B16F10 melanoma model by the change of dynamics of tumor growth (volume, mass) and its morphological structure (presence of necrotic processes, blood vessel destruction). The number of the effector immune cells (CD3+, CD11b+) in the tumor tissue was determined by immunohistochemical method.Results. It has been shown that VLP-TNF-α administered intravenously at the doses of 5 × 104 and 1 × 105 IU/mouse inhibits the growth of the primary tumor. The most pronounced and stable effect was observed with a five-fold administration at the dose of 1 × 105 IU/mouse every other day: tumor growth inhibition was 40 % on the 1st day, and 47 % on the 7 th day upon the treatment. Injections of the preparation resulted in the increase of necrosis number, destruction level of the tumor tissue, development of damage and destruction of the tumor blood vessels and its infiltration with immunocompetent cells.Conclusion. The obtained data indicates that TNF-α within the delivery system exerts antitumor activity, which suggests the possibility of its further use for the treatment of malignant neoplasms, in particular, melanoma.The study was performed in accordance with ethical principles adopted by the European Convention for the protection of vertebrate animals used for experimental and other scientific purposes.
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Popkin, Daniel L., and Herbert W. Virgin. "Murine Cytomegalovirus Infection Inhibits Tumor Necrosis Factor Alpha Responses in Primary Macrophages." Journal of Virology 77, no. 18 (September 15, 2003): 10125–30. http://dx.doi.org/10.1128/jvi.77.18.10125-10130.2003.
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ABSTRACT Despite robust host immune responses the betaherpesvirus murine cytomegalovirus (MCMV) is able to establish lifelong infection. This capacity is due at least in part to the virus utilizing multiple immune evasion mechanisms to blunt host responses. Macrophages are an important cell for MCMV infection, dissemination, and latency despite expression in the host of multiple cytokines, including tumor necrosis factor alpha (TNF-α), that can induce an antiviral state in macrophages or other cells. In this study, we found that MCMV infection of bone marrow-derived macrophages inhibited TNF-α-induced ICAM-1 surface expression and mRNA expression in infected cells via expression of immediate early and/or early viral genes. MCMV infection blocked TNF-α-induced nuclear translocation of NF-κB. This inhibition of TNF-α signaling was explained by a decrease in TNF receptor 1 (TNFR1) and TNFR2 that was due to decreased mRNA for the latter. These findings provide a mechanism by which MCMV can evade the effects of an important host cytokine in macrophages.
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Lavine, Sean D., Florence M. Hofman, and Berislav V. Zlokovic. "Circulating Antibody against Tumor Necrosis Factor–Alpha Protects Rat Brain from Reperfusion Injury." Journal of Cerebral Blood Flow & Metabolism 18, no. 1 (January 1998): 52–58. http://dx.doi.org/10.1097/00004647-199801000-00005.
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The role of tumor necrosis factor-alpha (TNF-α) in brain injury is controversial. We studied the effect of anti–TNF-α antibody in a rat model of reversible middle cerebral artery occlusion. During focal ischemia and early reperfusion, TNF-α was rapidly and transiently released into circulation. Pretreatment with intravenous anti–TNF-α antibody reduced cortical (71%, P < 0.015) and subcortical (58%, P < 0.007) injury, enhanced the cerebral blood flow during reperfusion, and improved the neurologic outcome. This further supports the contention that TNF-α is a deleterious cytokine in stroke, whereas circulating antibody against TNF-α may protect brain from reperfusion injury.
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Allan-Yorke, Justine, Michel Record, Claude de Préval, Christian Davrinche, and Jean-Luc Davignon. "Distinct Pathways for Tumor Necrosis Factor Alpha and Ceramides in Human Cytomegalovirus Infection." Journal of Virology 72, no. 3 (March 1, 1998): 2316–22. http://dx.doi.org/10.1128/jvi.72.3.2316-2322.1998.
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ABSTRACT Human cytomegalovirus (HCMV) infection can be fatal to immunocompromised individuals. We have previously reported that gamma interferon and tumor necrosis factor alpha (TNF-α) synergistically inhibit HCMV replication in vitro. Ceramides have been described as second messengers induced by TNF-α. To investigate the mechanisms involved in the inhibition of HCMV by TNF-α, in the present study we have analyzed ceramide production by U373 MG astrocytoma cells and the effects of TNF-α versus ceramides on HCMV replication. Our results show that U373 MG cells did not produce ceramides upon incubation with TNF-α. Moreover, long-chain ceramides induced by treatment with exogenous bacterial sphingomyelinase inhibited HCMV replication in synergy with TNF-α. Surprisingly, short-chain permeant C6-ceramide increased viral replication. Our results show that the anti-HCMV activity of TNF-α is independent of ceramides. In addition, our results suggest that TNF-α and endogenous long-chain ceramides use separate pathways of cell signalling to inhibit HCMV replication, while permeant C6-ceramide appears to activate a third pathway leading to an opposite effect.
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YAMASHITA, Satoyoshi. "Possible role of tumor necrosis factor-.ALPHA. for induction of hepatic cell necrosis." Kanzo 32, no. 4 (1991): 384–92. http://dx.doi.org/10.2957/kanzo.32.384.
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Khaiboullina, Svetlana F., Dale M. Netski, Peter Krumpe, and Stephen C. St. Jeor. "Effects of Tumor Necrosis Factor Alpha on Sin Nombre Virus Infection In Vitro." Journal of Virology 74, no. 24 (December 15, 2000): 11966–71. http://dx.doi.org/10.1128/jvi.74.24.11966-11971.2000.
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ABSTRACT Previous data indicate that immune mechanisms may be involved in developing capillary leakage during Sin Nombre virus (SNV) infection. Therefore, we investigated production of tumor necrosis factor alpha (TNF-α) by human alveolar macrophages and human umbilical vein endothelial cells (HUVEC) after infection with SNV. In addition, we examined the effect of TNF-α on HUVEC monolayer leakage. Our results reveal that although TNF-α decreases accumulation of viral nucleoproteins, TNF-α levels do not change in SNV-infected cells. In addition, supernatants from SNV-infected human alveolar macrophages did not cause a significant increase in endothelial monolayer permeability.
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Simamora, Rona Hanani, Bahagia Loebis, and Muhammad Surya Husada. "Comparison of Serum Levels of Tumor Necrosis Factor Alpha (TNF-α) in Batak Male Schizophrenic Patients Versus Healthy Controls." International Journal of Life-Sciences Scientific Research 4, no. 2 (March 2018): 1652–56. http://dx.doi.org/10.21276/ijlssr.2018.4.2.6.
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Fontt, Elizabeth Olivares, Patrick De Baetselier, Carlo Heirman, Kris Thielemans, Ralph Lucas, and Bernard Vray. "Effects of Granulocyte-Macrophage Colony-Stimulating Factor and Tumor Necrosis Factor Alpha on Trypanosoma cruzi Trypomastigotes." Infection and Immunity 66, no. 6 (June 1, 1998): 2722–27. http://dx.doi.org/10.1128/iai.66.6.2722-2727.1998.
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ABSTRACT We have previously shown that the addition of exogenous granulocyte-macrophage colony-stimulating factor (GM-CSF) to nonactivated mouse peritoneal macrophages (MPM) limitsTrypanosoma cruzi infections in vitro (E. Olivares Fontt and B. Vray, Parasite Immunol. 17:135–141, 1995). Lower levels of infection were correlated with a higher level of production of tumor necrosis factor alpha (TNF-α) in the absence of nitric oxide (NO) release. These data suggested that GM-CSF and/or TNF-α might have a direct parasitocidal effect on T. cruzi trypomastigotes, independently of NO release. To address this question, T. cruzi trypomastigotes were treated with recombinant murine GM-CSF (rmGM-CSF), recombinant murine TNF-α (rmTNF-α), or both cytokines in a cell-free system. Treatment with rmGM-CSF but not rmTNF-α caused morphological changes in the parasites, and most became spherical after 7 h of incubation. Both cytokines exerted a cytolytic activity on the trypomastigotes, yet the trypanolytic activity of rmTNF-α was more effective than that of rmGM-CSF. Viable rmGM-CSF- and rmTNF-α-treated parasites were less able to infect MPM than untreated parasites, and this reduction in infectivity was greatest for rmGM-CSF. Treatments with both cytokines resulted in more lysis and almost complete inhibition of infection. The direct parasitocidal activity of rmTNF-α was inhibited by carbohydrates and monoclonal antibodies specific for the lectin-like domain of TNF-α. Collectively, these results suggest that cytokines such as GM-CSF and TNF-α may directly control the level of T. cruzi trypomastigotes at least in vitro and so could determine the outcome of infection in vivo.
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Rukmono, Prambudi, Nani Dharmasetiawani, Warsono Warsono, Yan Wirasti, and Eryati Darwin. "Tumor necrosis factor-alpha and interleukin-6 in early-onset neonatal sepsis." Paediatrica Indonesiana 56, no. 1 (May 12, 2016): 15. http://dx.doi.org/10.14238/pi56.1.2016.15-8.
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Background Neonatal sepsis remains a major cause of mortality and morbidity in newborns. Early-onset neonatal sepsis occurs in infants under the age of 72 hours, while late-onset neonatal sepsis occurs in infants over the age of 72 hours and may be due to nosocomial infection. Diagnosing neonatal sepsis is a challenge, as its clinical symptoms are not clear. Corroborating tests include routine blood, C-reactive protein (CRP), serology, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) examinations.Objective To compare the TNF-α and IL-6 levels in patients with proven and unproven early-onset neonatal sepsis (EONS)Methods This case-control study was done in the Perinatology Unit, Abdul Moeloek Hospital, Lampung. Subjects were under the age of 72 hours with risk factors and clinical symptoms of sepsis. They underwent routine blood tests and blood cultures. Infants with positive cultures were considered to have proven sepsis (26 subjects) and infants with negative blood cultures were considered to have unproven sepsis (26 subjects). All subjects underwent serological examinations of TNF-α and IL-6.Results There were no differences in the basic characteristics of subjects between the two groups. Levels of TNF-α in the sepsis group were significantly higher than in the unproven group [(28.30 vs. 10.96 pg/mL, respectively (P=0.001)]. Furthermore, Il-6 was significantly higher in the proven sepsis group than in the unproven sepsis group [(28.3 vs. 9.69 pg/mL, respectively) (P=0.006)].Conclusion Levels of TNF-alpha and IL-6 are significantly higher in infants with proven than unproven early-onset neonatal sepsis.
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Meng, Jufeng, Ke Xu, Yinyin Qin, Ya Liu, Lin Xu, Shigang Qiao, Jianzhong An, Jianjun Liu, and Zhenhao Zhang. "Tumor Necrosis Factor-Alpha Disrupts Cx43-Mediated Corneal Endothelial Gap Junction Intercellular Communication." Oxidative Medicine and Cellular Longevity 2022 (September 19, 2022): 1–9. http://dx.doi.org/10.1155/2022/4824699.
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Connexin43 (Cx43)-mediated gap junctions are vital in maintaining corneal endothelium homeostasis. Tumor necrosis factor-alpha (TNF-α) is among the most important inflammatory factors which cause corneal endothelial dysfunction in various eye diseases. However, the effect of TNF-α on Cx43-mediated gap junctions of the corneal endothelium remains undefined. In the current research, we determined the effect of TNF-α on gap junction intercellular communication (GJIC) in rabbit corneal endothelium. To evaluate alterations of GJIC, if any, we treated ex vivo cultured rabbit corneal endothelium with different concentrations of TNF-α (2-20 ng/ml). The localization of Cx43 was analyzed by immunostaining, while RT-qPCR and western blot were used to profile the expression of Cx43 and zonula occludens-1 (ZO-1). The association between ZO-1 and Cx43 was evaluated using immunoprecipitation and double staining. GJIC activity was determined by the scrap loading and dye transfer assay (SLDT). Our data demonstrated that a high concentration of TNF-α (10 ng/ml and 20 ng/ml) disrupts the Cx43 mediated gap junction distribution in rabbit corneal endothelium and suppresses the expression of Cx43 protein. Furthermore, rabbit corneal endothelial GJIC was inhibited due to the decreased association between the ZO-1 and Cx43 proteins. Current results demonstrate that TNF-α inhibits corneal endothelial GJIC via decreasing the association between ZO-1 and Cx43, disrupting the distribution of Cx43, and downregulating the expression of Cx43 protein. This study offers a new theoretical foundation for diagnosing and treating corneal endothelial cell decompensation induced by elevated TNF-α in various eye diseases.
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Kwon, Hyung-Joo, Erin Haag Breese, Eva Vig-Varga, Yong Luo, Younghee Lee, Mark G. Goebl, and Maureen A. Harrington. "Tumor Necrosis Factor Alpha Induction of NF-κB Requires the Novel Coactivator SIMPL." Molecular and Cellular Biology 24, no. 21 (November 1, 2004): 9317–26. http://dx.doi.org/10.1128/mcb.24.21.9317-9326.2004.
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ABSTRACT A myriad of stimuli including proinflammatory cytokines, viruses, and chemical and mechanical insults activate a kinase complex composed of IκB kinase β (IKK-β), IKK-α, and IKK-γ/N, leading to changes in NF-κB-dependent gene expression. However, it is not clear how the NF-κB response is tailored to specific cellular insults. Signaling molecule that interacts with mouse pelle-like kinase (SIMPL) is a signaling component required for tumor necrosis factor alpha (TNF-α)-dependent but not interleukin-1-dependent NF-κB activation. Herein we demonstrate that nuclear localization of SIMPL is required for type I TNF receptor-induced NF-κB activity. SIMPL interacts with nuclear p65 in a TNF-α-dependent manner to promote endogenous NF-κB-dependent gene expression. The interaction between SIMPL and p65 enhances p65 transactivation activity. These data support a model in which TNF-α activation of NF-κB dependent-gene expression requires nuclear relocalization of p65 as well as nuclear relocalization of SIMPL, generating a TNF-α-specific induction of gene expression.
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Richmond, Jillian M., Elizabeth R. Duffy, Jinhee Lee, Kavon Kaboli, Daniel G. Remick, Hardy Kornfeld, and William W. Cruikshank. "Mannose-Capped Lipoarabinomannan from Mycobacterium tuberculosis Induces Soluble Tumor Necrosis Factor Receptor Production through Tumor Necrosis Factor Alpha-Converting Enzyme Activation." Infection and Immunity 80, no. 11 (August 27, 2012): 3858–68. http://dx.doi.org/10.1128/iai.00060-12.
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ABSTRACTPrimaryMycobacterium tuberculosisinfection results in granuloma formation in lung tissue. A granuloma encapsulates mycobacterium-containing cells, thereby preventing dissemination and further infection. Tumor necrosis factor alpha (TNF-α) is a host-protective cytokine duringM. tuberculosisinfection due to its role in promoting and sustaining granuloma formation. TNF activity is regulated through the production of soluble TNF receptors (sTNFRI and sTNFRII). Therefore, we examined the potential production of endogenous sTNFRs duringM. tuberculosisinfection. Using the murine model of aerosolM. tuberculosisinfection, we determined that levels of sTNFR production were elevated in bronchoalveolar lavage fluid 1 month following infection. An investigation ofM. tuberculosiscell wall components identified that the known virulence factor mannose-capped lipoarabinomannan (ManLAM) was sufficient to induce sTNFR production, with sTNFRII being produced preferentially compared with sTNFRI. ManLAM stimulated the release of sTNFRs without TNF production, which corresponded to an increase in TNF-α-converting enzyme (TACE) activity. To determine the relevance of these findings, serum samples fromM. tuberculosis-infected patients were tested and found to have an increase in the sTNFRII/sTNFRI ratio. These data identify a mechanism by whichM. tuberculosisinfection can promote the neutralization of TNF and furthermore suggest the potential use of the sTNFRII/sTNFRI ratio as an indicator of tuberculosis disease.
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Ciacci-Woolwine, Federica, Ian C. Blomfield, Stephen H. Richardson, and Steven B. Mizel. "Salmonella Flagellin Induces Tumor Necrosis Factor Alpha in a Human Promonocytic Cell Line." Infection and Immunity 66, no. 3 (March 1, 1998): 1127–34. http://dx.doi.org/10.1128/iai.66.3.1127-1134.1998.
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ABSTRACT During infection of the gastrointestinal tract, salmonellae induce cytokine production and inflammatory responses which are believed to mediate tissue damage in the host. In a previous study, we reported that salmonellae possess the ability to stimulate tumor necrosis factor alpha (TNF-α) accumulation in primary human monocytes, as well as in the human promonocytic cell line U38. In this model system, cytokine upregulation is not due to lipopolysaccharide but is mediated by a released protein. In the present study, TnphoA transposon mutagenesis was used to identify the TNF-α-inducing factor. A mutantSalmonella strain which lacks the ability to induce TNF-α was isolated from a TnphoA library. Genetic analysis of this mutant demonstrated that the hns gene has been interrupted by transposon insertion. The hns gene product is a DNA-binding protein that regulates the expression of a variety of unrelated genes in salmonellae. One of the known targets of histone-like protein H1 is flhDC, the master operon which is absolutely required for flagellar expression. Analysis of other nonflagellated mutant Salmonella strains revealed a correlation between the ability to induce TNF-α and the expression of the phase 1 filament subunit protein FliC. Complementation experiments demonstrated that FliC is sufficient to restore the ability of nonflagellated mutant Salmonella strains to upregulate TNF-α, whereas the phase 2 protein FljB appears to complement to a lesser extent. In addition, Salmonella FliC can confer the TNF-α-inducing phenotype on Escherichia coli, which otherwise lacks the activity. Furthermore, assembly of FliC into complete flagellar structures may not be required for induction of TNF-α.
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Roșu, Mihai Cătălin, Petrut Dinu Mihnea, Andrei Ardelean, Silviu Daniel Moldovan, Romana Olivia Popețiu, and Bogdan Dan Totolici. "Clinical significance of tumor necrosis factor-alpha and carcinoembryonic antigen in gastric cancer." Journal of Medicine and Life 15, no. 1 (January 2022): 4–6. http://dx.doi.org/10.25122/jml-2020-0098.
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Tumour necrosis factor (TNF)-α plays an important role in inflammatory, infectious, and tumor processes, and it is closely related to the early stages of gastric cancer. It is a pro-inflammatory cytokine, produced not only by macrophages and monocytes but also by the lymphocytes, mast cells, neutrophils, keratinocytes, smooth muscle cells, and some tumor cell lines. Large amounts of TNF are released upon contact of macrophages, CD4 + T lymphocytes, and natural killer (NK) cells with lipopolysaccharides, bacterial products, and interleukin 1. TNF-alpha inducing protein (Tipa) is a unique carcinogenic factor of Helicobacter pylori, secreted into culture broth. The biological activities of TNF alpha and deletion mutant were studied. TNF alpha protein specifically binds to cell-surface nucleolin and then enters the gastric cancer cells, where TNF-a and chemokine gene expressions are induced by NF-jB activation. Nucleolin localizes on the surface of gastric cancer cells, and interaction between TNF alpha and cell-surface nucleolin causes a cancer-oriented microenvironment that increases the risk of gastric cancer. This paper discusses a mechanism of gastric cancer development and the clinical significance of tumor necrosis-alpha and carcinoembryonic antigen in gastric cancer.
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Gómez del Moral, M., E. Ortuño, P. Fernández-Zapatero, F. Alonso, C. Alonso, A. Ezquerra, and J. Domínguez. "African Swine Fever Virus Infection Induces Tumor Necrosis Factor Alpha Production: Implications in Pathogenesis." Journal of Virology 73, no. 3 (March 1, 1999): 2173–80. http://dx.doi.org/10.1128/jvi.73.3.2173-2180.1999.
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ABSTRACT We have analyzed the production of tumor necrosis factor alpha (TNF-α) induced by in vitro infection with African swine fever (ASF) virus (ASFV) and the systemic and local release of this inflammatory cytokine upon in vivo infection. An early increase in TNF-α mRNA expression was detected in ASFV-infected alveolar macrophages, and high levels of TNF-α protein were detected by ELISA in culture supernatants from these cells. When animals were experimentally infected with a virulent isolate (E-75), enhanced TNF-α expression in mainly affected organs correlated with viral protein expression. Finally, elevated levels of TNF-α were detected in serum, corresponding to the onset of clinical signs. TNF-α has been reported to be critically involved in the pathogenesis of major clinical events in ASF, such as intravascular coagulation, tissue injury, apoptosis, and shock. In the present study, TNF-α containing supernatants from ASFV-infected cultures induced apoptosis in uninfected lymphocytes; this effect was partially abrogated by preincubation with an anti-TNF-α specific antibody. These results suggest a relevant role for TNF-α in the pathogenesis of ASF.
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O’Brien, David P., David E. Briles, Alexander J. Szalai, Anh-Hue Tu, Inaki Sanz, and Moon H. Nahm. "Tumor Necrosis Factor Alpha Receptor I Is Important for Survival from Streptococcus pneumoniaeInfections." Infection and Immunity 67, no. 2 (February 1, 1999): 595–601. http://dx.doi.org/10.1128/iai.67.2.595-601.1999.
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ABSTRACT Tumor necrosis factor alpha (TNF-α) is important in resistance to various microorganisms and provides signals to the target cells through two different receptors, TNF-α receptor I (TNFRI) (p55 receptor) and TNFRII (p75 receptor). To delineate the significance of the two different signaling pathways in resisting infections with extracellular bacteria, we examined the resistance of mice to Streptococcus pneumoniae (serotype 6B). TNF-α needs to be present early in infections, since one injection of wild-type mice with anti-TNF-α leads to an increased susceptibility of these mice to S. pneumoniae. TNF-α signaling through the p55 receptor (but not the p75 receptor) is crucial in resisting S. pneumoniae infections, because intraperitoneal injection of 100 CFU/mouse killed p55-deficient mice by day 2 of infection, whereas 1,000,000 CFU/mouse was needed to kill half of the control mice. p55-deficient mice do not show evidence of a deficient acute-phase response. All three types of mice (p55 deficient, p75 deficient, and normal) showed comparable rises in the levels of two acute-phase proteins (serum amyloid P and C3) at 24, 48, and 72 h after the experimental infections, and all of the mice showed comparable influxes of neutrophils to the site of infection. Finally, it was demonstrated that p55-deficient mice can be protected from the lethal effects of S. pneumoniae infection by injection of antibodies specific for S. pneumoniaepolysaccharide capsule.
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Masukawa, Ena, Yoshiaki Matsushima, Koji Habe, and Keiichi Yamanaka. "Two Cases of Cutaneous Adverse Effects Induced by Tumor Necrosis Factor-Alpha Inhibitors." Case Reports in Dermatology 13, no. 1 (April 19, 2021): 238–43. http://dx.doi.org/10.1159/000511985.
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Here, we report two cases of cutaneous adverse effects possibly induced by the use of tumor necrosis factor-alpha (TNF-α) inhibitors. The first case presented alopecia areata (AA) and atopic dermatitis (AD) that developed during the treatment of ulcerative colitis using infliximab; the other case presented urticaria and AD that developed during the treatment of rheumatoid arthritis using etanercept. AA, AD, and urticaria are relatively common skin diseases; however, they are not well known as adverse effects of TNF-α inhibitors. Although immunological studies were not performed, the clinical courses suggested that these skin disorders might have developed as a result of an immune four-way imbalance in T helper 1 (Th1), Th2, Th17, and regulatory T cells by the administration of TNF-α inhibitors.
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Abbas, Ahmed Abdul-Hassan, Zainab J. Fadhil, and Shatha Hussein Ali. "Tumor Necrosis Factor Alpha-863 C/A Single Nucleotide Polymorphisms and Nephrotic Syndrome." International Journal of Drug Delivery Technology 10, no. 03 (September 25, 2020): 319–22. http://dx.doi.org/10.25258/ijddt.10.3.1.
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Introduction: Cytokines act as a mediator of inflammation in childhood nephrotic syndrome. Polymorphisms of cytokines genes may influence susceptibility to nephrotic syndrome (NS), as well as, patients’ steroid responses. Objective: To study the association of tumor necrosis factor-alpha single nucleotide polymorphisms (TNF-α SNP) (-863 C/A) with the development of NS in addition to access to their effects on serum level of TNF and the response to steroid therapy. Patients and Methods: This study included 60 patients (19 female and 41 male) with nephrotic syndrome; their ages ranged from 2 to 18 years. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to assess the TNF-α gene polymorphism. Results: According to the digestion pattern of RFLP-PCR products of TNF-α-863, this polymorphism had three genotypes, which were CC, CA, and AA, in both NS patients and controls. Also, the current result observed that -863 SNP do not affect the serum level of TNF-α and steroid responsiveness in patients with nephrotic syndrome. Conclusion: This polymorphism did not show any significant association with response to steroid therapy and TNF serum level neither at genotype nor at allele level.