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Abstract: Introduction: The P2X7 receptor‐NLRP3 inflammasome complex (P2X7R‐Infl) regulates inflammatory and immune responses. Physical exercise modulates heat‐shock proteins (Hsps), influencing cytokine levels and oxidative stress; Hsp72 triggers P2X7R‐Infl‐dependent responses. Subjects and Methods: We studied the effect of a single bout of maximal exercise on lymphomonocyte expression of P2X7R, NLRP3, caspase‐1, NF‐kB and Hsp72 and circulating levels of IL‐1β, IL‐18 and MCP‐1, all modulated by P2X7R‐Infl, in healthy sedentary (SED), trained (ATH), endurance (END) male individuals. Results: Baseline P2X7R, NLRP3 and Caspase‐1 expression progressively increased from SED to ATH and END; NF‐kβ showed the same trend. Hsp72 did not differ among groups. Acute exercise strongly reduced P2X7R in all participants, irrespective of their degree of physical training. Inflammasome responses differed across groups: in SED, NLRP3 and Caspase‐1 increased; in ATH, NLRP3 reduced and caspase‐1 did not vary; in END, NLRP3 and Caspase‐1 declined. Baseline IL‐1β, higher in END, was unmodified after exercise; IL‐18 decreased; MCP‐1 doubled in SED, did not vary in ATH, declined in END. In the whole study population, significant direct relationships emerged between P2X7R expression and IL‐1β, IL‐18, MCP‐1 levels, all P < .001; also Caspase‐1 related with these markers. A multivariate analysis showed age, BMI and P2X7R as determinants of postexercise IL‐1β levels. Conclusion: Endurance show higher P2X7R‐Infl expression and function vs SED and ATH; however, maximal exercise determines prevailing pro‐inflammatory vs anti‐inflammatory responses in untrained and trained participants, respectively, highlighting a likely cause‐effect relationship between degree of physical activity and P2X7R‐Infl‐mediated responses. [ABSTRACT FROM AUTHOR]

We present a rare cause of iridocyclitis in a patient with vitiligo and type 1 diabetes who showed poor metabolic control, and suffered from remitting fever, weight loss, fatigue, diffuse arthralgias and reduced visual acuity. Mild systemic symptoms coupled with increased cholestasis enzymes, insulin resistance, mild inflammation and a functioning adrenal gland focused our clinical work-up on granulomatous causes of iridocyclitis. Specific tests confirmed syphilis, with no involvement of the central nervous system. Ocular syphilis, despite being unusual, can be the only manifestation of the disease. The work-up of any unexplained ocular inflammation should include testing for syphilis so as to not delay the diagnosis. [ABSTRACT FROM AUTHOR]

Objective Smoking is a recognized cardiovascular risk factor. Perivascular visceral adipose tissue ( PVAT) is a source of inflammatory molecules, thus contributing to atherosclerosis progression. The P2 X7 receptor ( P2 X7 R)-inflammasome complex, crucial in determining IL-1β and IL-18 release, participates in this scenario. We evaluated whether smoking might affect the PVAT inflammatory phenotype and explored the putative role of the axis P2 X7 R-inflammasome in this picture. Subjects and Methods TNFα, IL-6, RBP4, MCP-1, as well as P2 X7 R and inflammasome components NLRP3, ASC, caspase-1 and IL-1β and IL-18 expression was determined in adipocytes isolated by PVAT of healthy smokers ( Smok) and nonsmokers ( No- Smok) subjects. Plasma and culture medium levels of these cytokines were also determined. Results Perivascular adipose tissue of Smok had a higher expression of P2 X7 R and inflammasome components; via P2 X7 R activation, it released more IL-1β and IL-18, whose serum levels were also higher in Smok than in No- Smok. Linear correlations of NLRP3 with P2 X7 R and IL-18 expression and release emerged. Smok also had a higher PVAT expression of the chemotactic factor MCP-1. However, no difference was observed in the PVAT expression of genes more strictly related to insulin resistance, like TNFα, RBP4, IL-6; this was coupled with similar plasma levels of TNFα and RBP4 in the two groups. Conclusion Smoking contributes to the pro-inflammatory status of the PVAT by enhancing expression and activity of the P2 X7 R-inflammasome complex; the effect on adipocytokines more related to insulin resistance and metabolic abnormalities appears trivial. [ABSTRACT FROM AUTHOR]