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Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact. Aim The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR. Subjects and methods An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people. Results Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV. Conclusion There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.

The aim of this study was to determine the effects of gallium arsenide (GaAs) laser on IGF-I, MyoD, MAFbx, and TNF-α gene expression during the intermediate phase of muscle regeneration after cryoinjury 21 Wistar rats were divided into three groups (n = 7 per group): untreated with no injury (control group), cryoinjury without GaAs (injured group), and cryoinjury with GaAs (GaAs-injured group). The cryoinjury was induced in the central region of the tibialis anterior muscle (TA). The region injured was irradiated once a day during 14 days using GaAs laser (904 nm; spot size 0.035 cm2, output power 50 mW; energy density 69 J cm−2; exposure time 4 s per point; final energy 4.8 J). Twenty-four hours after the last application, the right and left TA muscles were collected for histological (collagen content) and molecular (gene expression of IGF-I, MyoD, MAFbx, and TNF-α) analyses, respectively. Data were analyzed using one-way ANOVA at P < 0.05. There were no significant (P > 0.05) differences in collagen density and IGF-I gene expression in all experimental groups. There were similar (P < 0.05) decreases in MAFbx and TNF-α gene expression in the injured and GaAs-injured groups, compared to control group. The MyoD gene expression increased (P = 0.008) in the GaAs-injured group, but not in the injured group (P = 0.338), compared to control group. GaAs laser therapy had a positive effect on MyoD gene expression, but not IGF-I, MAFbx, and TNF-α, during intermediary phases (14 days post-injury) of muscle repair.

Background Tumor necrosis factor plays a critical role in the pathogenesis of gastric diseases such as gastric cancer, and an abnormal inflammatory response has frequently been observed in dyspeptic patients. Helicobacter pylori infection can induce a gastric mucosal inflammatory response that may be influenced by -308 (G > A) polymorphisms and gene expression of the TNF -α gene. Methods One hundred and thirty-four gastric biopsy samples were collected from patients of both genders (61♂ and 73♀, mean age 40.3 ± 24.2 years) with gastric symptoms. The -308 (G > A) polymorphism of TNF -α was characterized using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The expression level was measured using real-time PCR, and relative quantification (RQ) was calculated using the comparative CT method (2 -ΔΔCT ). Results The analysis revealed an increase in TNF -α gene expression in patients with gastritis; on the other hand, no statistical differences were observed in patients with gastric cancer. In addition, no association was found among -308 polymorphism genotypes, virulence markers, or TNF -α gene expression. Conclusions Helicobacter pylori induces a large increase in TNF - α expression in patients with gastritis, regardless of tissue inflammation, but after the tissue becomes neoplastic, the presence of bacteria did not influence expression. These results suggest that the TNF- α pathway may play an important role in the progression from gastritis to gastric cancer

TNF-α is postulated to play a significant role in regulating TGF-β 1 expression. In lung fibroblasts, for example, TNF-α is supposed to induce TGF-β 1 via AP-1 activation. TNF-α receptor, knock-out mice are resistant to induced fibrosis and over-expression of TNF-α causes increased TGF-β 1 production in mice. Therefore, we investigated whether TNF-α mRNA levels are associated with the TGF-β 1 mRNA levels of blood leucocytes in humans. Quantitative real-time PCR of TNF-α and TGF-β 1 was performed in 118 Germans. Calculations of expression were made with the 2 −ΔΔCT method. When the investigated population was divided in two groups (TNF-α low and TNF-α high) by the median of the determined TNF-α expression, highly significant ( p  < 0.0001) differences of TGF-β1 mRNA expression were revealed. Additionally, dividing the investigated population into quartiles of the determined TNF-α expression showed significantly different TGF-β1 mRNA expressions. Comparing the determined CT-values of TNF-α in context with these of TGF-β1, a coefficient of determination R 2  = 0.4635 was calculated. In this study we demonstrated in vivo a significant association of the relative TNF-α/B2M mRNA expression and the relative TGF-β 1 /B2M mRNA expression in 118 Germans.

The aim of the study was to research the biological functions of circRNA (hsa_circ_0079662) and its underlying mechanism in colorectal cancer. Drug‐resistant cell lines (HT29‐LOHP, HCT116‐LOHP, HCT8‐LOHP) were separately dealt with oxaliplatin concentration gradient (0.1‐10 μmol/L). Real‐time PCR, Western blotting, dual‐luciferase assay, miRNA pull‐down assay, coimmunoprecipitation and ELASA were performed to explore the mechanism of chemotherapy drug oxaliplatin resistance in CRC. The results showed that the expression of hsa_circ_0079662 was increased in drug‐resistant cell lines by RT‐PCR. The expression of HOXA9, TRIP6, Vcam‐1, VEGFC, MMP3, MMP9 and MMP14 was higher by Western blotting. Interaction between HOXA9 and TRIP6 in CO‐IP detection. Additionally, the cytokines TNF‐α, IL‐1 and IL‐6 were also found. In conclusion, hsa_circ_0079662, as a ceRNA binding with hsa‐mir‐324‐5p, can regulate target gene HOXA9 and induced the mechanism of chemotherapy drug oxaliplatin resistance in CRC through the TNF‐α pathway in human colon cancer.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic systemic inflammation causing progressive joint damage that can lead to lifelong disability. The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.

Immunotherapy using anti‐PD‐1/PD‐L1 antibodies for several types of cancer has received considerable attention in recent decades. However, the molecular mechanism underlying PD‐L1 expression in pancreatic ductal adenocarcinoma (PDAC) cells has not been clearly elucidated. We investigated the clinical significance and regulatory mechanism of PD‐L1 expression in PDAC cells. Among the various cytokines tested, tumor necrosis factor (TNF)‐α upregulated PD‐L1 expression in PDAC cells through NF‐κB signaling. The induction of PD‐L1 expression was also caused by co‐culture with activated macrophages, and the upregulation was inhibited by neutralization with anti‐TNF‐α antibody after co‐culture with activated macrophages. PD‐L1 expression in PDAC cells was positively correlated with macrophage infiltration in tumor stroma of human PDAC tissues. In addition, survival analysis revealed that high PD‐L1 expression was significantly associated with poor prognosis in 235 PDAC patients and especially in patients harboring high CD8‐positive T‐cell infiltration. These findings indicate that tumor‐infiltrating macrophage‐derived TNF‐α could be a potential therapeutic target for PDAC. Survival analysis revealed that PD‐L1 expression was significantly associated with poor prognosis in PDAC patients and especially in patients harboring high CD8‐positive T‐cell infiltration. The induction of PD‐L1 expression was caused by co‐culture with activated macrophages, and the upregulation was inhibited by neutralization with anti‐TNF‐α antibody after co‐culture with activated macrophages.

Cytokines and chemokines represent two important groups of proteins that control the human immune system. Dysregulation of the network in which these immunomodulators function can result in uncontrolled inflammation, leading to various diseases including rheumatoid arthritis (RA), characterized by chronic inflammation and bone erosion. Potential triggers of RA include autoantibodies, cytokines and chemokines. The tight regulation of cytokine and chemokine production, and biological activity is important. Tumor necrosis factor‐α (TNF‐α) is abundantly present in RA patients’ serum and the arthritic synovium. This review, therefore, discusses first the role and regulation of the major proinflammatory cytokine TNF‐α, in particular the regulation of TNF‐α production, post‐translational processing and signaling of TNF‐α and its receptors. Owing to the important role of TNF‐α in RA, the TNF‐α‐producing cells and the dynamics of its expression, the direct and indirect action of this cytokine and possible biological therapy for RA are described.