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BACKGROUND: Inflammatory cytokines play roles in the pathogenesis of celiac disease. To introduce new diagnostic markers in patients with celiac disease for easy, fast, low cost, and non-invasive diagnosis, we evaluated the peripheral blood expression levels of interleukin-15 (IL-15), interleukin-17A (IL-17A), interleukin23A (IL-23A), granzyme B (GzmB), T-box transcription factor 21 (TBX21), and tumor necrosis factor alpha-induced protein 3 (TNFAIP3) of patients compared with the healthy controls, which were extracted from public databases organized in a protein-protein interaction network, in this group. METHODS: Peripheral blood mononuclear cells were collected from 30 patients with celiac disease and 30 healthy subjects. Total RNA was extracted, and mRNA expression levels of targeted genes were investigated by the quantitative realtime polymerase chain reaction (PCR) method. SPSS software was used for statistical analysis. Receiver operating characteristic (ROC) curve analysis was performed to characterize the diagnostic ability of the studied genes. RESULTS: The expression of IL-15, IL-17A, IL-23A, GzmB, TBX21, and TNFAIP3 genes in peripheral blood mononuclear cells of patients with celiac disease showed a significant increase compared with the control group. Among them, TNFAIP3, IL23A, and GzmB have better resolution and diagnostic value in differentiating patients with celiac disease from healthy controls. CONCLUSION: Our results suggest that TNFAIP3, IL23A, and GzmB could be useful and sensible markers in differentiating patients with celiac disease from healthy controls. However, the diagnostic relevance of other genes recognized by pathway analysis needs to be further investigated. [ABSTRACT FROM AUTHOR]

BACKGROUND: Interaction between immune modulators and inflammatory factors is considered as one of the main underlying pathologies of non-alcoholic fatty liver disease (NAFLD). Hence we aimed to assess the association between these cytokines and melatonin. METHODS: We enrolled adult patients diagnosed with fatty liver by ultrasonography in a cross-sectional study. All of them underwent Fibroscan evaluation. The subjects who met the inclusion and exclusion criteria for NAFLD were involved. A normal group who did not have NAFLD, viral or non-viral hepatitis, and without a history of pancreatobiliary surgery, bariatric surgery, and intake of any medication that influence the liver was also selected. The participants were categorized into the three following groups: 1) fibrosis > 9.1 kPa and steatosis > 290 dbm, 2) fibrosis: 6-9.0 kPa and steatosis 240-290 dbm, and 3) normal group with fibrosis < 6.0 kPa and steatosis < 240 dbm. Laboratory assessment and a questionnaire including demographic, anthropometric, laboratories, and clinical data were completed for each of them. RESULTS: Totally 97 subjects were enrolled in the present study. The mean age of the subjects was 42.2 ± 11.3 years. 60% of them (59 patients) were female. Serum levels of melatonin, interleukin (IL)-1B, IL-18, and IL-33 increased according to the advancing of NAFLD state. Based on multiple linear regression model, melatonin was significantly associated with IL-1B (β = 2.8, P < 0.001,95% CI = 1.41-4.19), IL-18 (β = 0.018, P = 0.0005, 95% CI = 0.006-0.03), and IL-33 (β = 0.31, P = 0.045, 95% CI = 0.008-0.62) after adjustment for other variables. CONCLUSION: Melatonin level has a strong association with these cytokines. This linkage probably influences on the development and progression of NAFLD. Therefore it can be hypothesized that the therapeutic approach that affects this process may have a significant impact. [ABSTRACT FROM AUTHOR]

BACKGROUND: Parkinson's disease is a neurodegenerative disorder characterized by degeneration of dopaminergic neurons in the substantia nigari. Previous studies have shown that Helicobacter pylori (H. pylori) infection is associated with treatment and clinical response to Parkinson's disease. In the present study, we aimed to investigate the effect of H. pylori infection in the pathogenesis of Parkinson's disease. METHODS: 75 patients who suffered from Parkinson's disease and H. pylori infection and 91 healthy controls were recruited. All the subjects were evaluated for serum IgM, IgG, and IgA antibodies as well as TNF-α, IL-6, and IL-4 cytokines by Enzyme-Linked ImmunoSorbent Assay (ELISA)methods. RESULTS: The participants included 102 men and 64 women with a mean age of 66 ± 10.2 and 52.6 ± 10.7 years in the patients and control groups, respectively. The level of IgG, TNF-α, IL-6 in the patients with Parkinson's infected with H. pylori was significantly more than that in the control group. In contrast, IgA was significantly lower in patients with Parkinson's disease compared with the control group. CONCLUSION: Probably, persistent infection with H. pylori could be effective in the pathogenesis of Parkinson's disease by dominating the systemic inflammatory profile. It is suggested that pro-inflammatory cytokines followed by H. pylori infection through the promotion of immune response or neurotoxicity might have a role in the pathogenesis of Parkinson's disease. [ABSTRACT FROM AUTHOR]

BACKGROUND Understanding the associations among different disorders remarkably improves their diagnosis and treatments. Celiac disease is the most complicated and prevalent form of immune-mediated diseases. On the other hand, inflammatory bowel diseases lead to inflammation of the intestine with an unknown cause. Although inflammatory bowel diseases have been often thought of as an autoimmune disorder, they can be triggered by whatever that can lead to the inflammation in the whole bowel. Henceforth, both aforementioned diseases are related to autoimmune attacks and cause a sort of inflammatory event, which exploring trade-off among them supposedly will lead to discovering important genes and, in turn, to the possible common therapeutic protocols. In the current study, we aimed to determine the correlation between the common genes in celiac disease and inflammatory bowel diseases. METHODS 314 and 851 genes correlated with celiac disease and inflammatory bowel diseases respectively extracted from DisGeNET were subjected to an in-silico data analysis framework to mine prognosticates genes and the associated pathways. RESULTS 149 shared genes between these diseases regulated by highlighted transcription factors NFKB1, IRF1, STAT1, HSF1, GATA3 were characterized as discriminating molecules, which by further screening were enriched in pathways mostly involved in apoptosis, T cell activation, and cytokine, chemokine, and interleukin signaling. CONCLUSION We observed that the identified common genes were associated with a wide range of pathogenic mechanisms underlying these diseases. [ABSTRACT FROM AUTHOR]

BACKGROUND T cells are major players in chronic inflammatory diseases such as autoimmune hepatitis (AIH). However, it is not clear which subset of T cells participates in the pathophysiology of the disease. The aim of this study was to assess the expression profile of signature transcription factor and cytokines of T helper 17 (Th17) cells in patients with AIH. METHODS A total of 24 patients with AIH and 24 normal subjects were recruited in the study. Comparison of gene expression patterns between the patients and normal subjects was done by quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR). RESULTS The results showed that retinoic acid receptor-related orphan receptors gamma (RORγt), interleukin-17A (IL-17A), and interleukin-22 (IL-22) mRNA expression were increased greatly in the patients group compared with the normal controls group (p < 0.05). CONCLUSION Deregulated production of Th17-related molecules may be associated with the pathogenesis of AIH. [ABSTRACT FROM AUTHOR]