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This study evaluated the association between ultra-processed foods (UPF) on serum IL-6 and to investigate the mediation role of adiposity. Participants were 524 adults from the EPITeen Cohort (Porto, Portugal) and 2888 participants from the 1982 Pelotas Birth Cohort (Pelotas, Brazil). Dietary intake was collected using FFQ when participants were 21 years of age in the EPITeen and 23 years in the Pelotas Cohort. Serum IL-6 and body fat mass were evaluated when participants were 27 and 30 years old in the EPITeen and Pelotas, respectively. Generalised linear models were fitted to test main associations. Mediation of body fat mass was estimated using G-computation. After adjustment for socio-economic and behaviour variables, among females from the EPITeen, the concentration of IL-6 (pg/ml) increased with increasing intake of UPF from 1·31 (95 % CI 0·95, 1·82) in the first UPF quartile to 2·20 (95 % CI 1·60, 3·01) and 2·64 (95 % CI 1·89, 3·69) for the third and fourth UPF quartiles, respectively. A similar result was found among males in the Pelotas Cohort, IL-6 increased from 1·40 (95 % CI 1·32, 1·49) in the first UPF quartile to 1·50 (95 % CI 1·41, 1·59) and 1·59 (95 % CI 1·49, 1·70) in the two highest UPF quartiles. The P -value for the linear trend was < 0·01 in both findings. The indirect effect through fat mass was NS. Our findings suggest that the consumption of UPF was associated with an increase in IL-6 concentration; however, this association was not explained by adiposity. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) is one of the most common types of cancer among men, and coffee is associated with a reduced risk of developing PCa. Therefore, we aim to review possible coffee molecular mechanisms that contribute to PCa prevention. Coffee has an important antioxidant capacity that reduces oxidative stress, leading to a reduced mutation in cells. Beyond direct antioxidant activity, coffee stimulates phase II enzymatic activity, which is related to the detoxification of reactive metabolites. The anti-inflammatory effects of coffee reduce tissue damage related to PCa development. Coffee induces autophagy, regulates the NF-κB pathway, and reduces the expression of iNOS and inflammatory mediators, such as TNF-α, IL-6, IL-8, and CRP. Also, coffee modulates transcriptional factors and pathways. It has been shown that coffee increases testosterone and reduces sex hormone-binding globulin, estrogen, and prostate-specific antigen. Coffee also enhances insulin resistance and glucose metabolism. All these effects may contribute to protection against PCa development. [ABSTRACT FROM AUTHOR]

Objectives. Rheumatoid arthritis affects about 1% of the world's population. This is a chronic autoimmune disease. It is predominant in females with progressive joint damage. Immune cells are involved, especially Th1/Th17 lymphocytes and their inflammatory cytokines. These proteins have different functions in the immune system, such as IL-16 is a chemotactic factor; IL-18 can activate NFκB transcription producing inflammatory proteins; IL-31 can activate the JAK/STAT pathway which leads to the production of inflammatory factors in chronic diseases; IL-33 promotes IL-16 secretion which causes lymphocyte recruitment, and IL-32 and IL-34 appear to increase TNF secretion by macrophages activation in AR.Theaim of this study was to evaluate serum levels of IL-16, IL-18, IL-31, IL-32, IL-33, and IL-34 and compare them with the severity and treatment of RA patients if there are any correlations. Methods. A total of 140 RA patients and 40 healthy donors were recruited from the Department of Rheumatology at Hospital das Cl'ınicas from the Federal University of Pernambuco. 60 AR patients were naïve for any treatment. Serum cytokine levels were determined using an ELISA kit. Results. Serum IL-16 (p = 0.0491), IL-18 (p < 0.0001), IL-31 (p = 0.0004), and IL-32 (p = 0.0040) levels were significantly increased in RA patients compared with healthy donors. It was observed that patients using leflunomide had the lowest IL-18 levels, close to controls levels (p = 0.0064). Conclusion. IL-16, IL-18, IL-31, and IL-32 are increased in the serum of RA patients. IL-18 is at lower levels in those AR who are taking leflunomide as treatment. [ABSTRACT FROM AUTHOR]

Background: Acute inflammatory reactions are a frequently occurring, tissue destructing phenomenon in infectious- as well as autoimmune diseases, providing clinical challenges for early diagnosis. In leprosy, an infectious disease initiated by Mycobacterium leprae (M. leprae), these reactions represent the major cause of permanent neuropathy. However, laboratory tests for early diagnosis of reactional episodes which would significantly contribute to prevention of tissue damage are not yet available. Although classical diagnostics involve a variety of tests, current research utilizes limited approaches for biomarker identification. In this study, we therefore studied leprosy as a model to identify biomarkers specific for inflammatory reactional episodes.Methods: To identify host biomarker profiles associated with early onset of type 1 leprosy reactions, prospective cohorts including leprosy patients with and without reactions were recruited in Bangladesh, Brazil, Ethiopia and Nepal. The presence of multiple cyto-/chemokines induced by M. leprae antigen stimulation of peripheral blood mononuclear cells as well as the levels of antibodies directed against M. leprae-specific antigens in sera, were measured longitudinally in patients.Results: At all sites, longitudinal analyses showed that IFN-γ-, IP-10-, IL-17- and VEGF-production by M. leprae (antigen)-stimulated PBMC peaked at diagnosis of type 1 reactions, compared to when reactions were absent. In contrast, IL-10 production decreased during type 1 reaction while increasing after treatment. Thus, ratios of these pro-inflammatory cytokines versus IL-10 provide useful tools for early diagnosing type 1 reactions and evaluating treatment. Of further importance for rapid diagnosis, circulating IP-10 in sera were significantly increased during type 1 reactions. On the other hand, humoral immunity, characterized by M. leprae-specific antibody detection, did not identify onset of type 1 reactions, but allowed treatment monitoring instead.Conclusions: This study identifies immune-profiles as promising host biomarkers for detecting intra-individual changes during acute inflammation in leprosy, also providing an approach for other chronic (infectious) diseases to help early diagnose these episodes and contribute to timely treatment and prevention of tissue damage. [ABSTRACT FROM AUTHOR]