Summary: Crohn's disease (CD) has been correlated with altered macrophage response to microorganisms. Considering the efficacy of infliximab treatment on CD remission, we investigated infliximab effects on circulating monocyte subsets and on macrophage cytokine response to bacteria. Human peripheral blood monocyte-derived macrophages were obtained from CD patients, treated or not with infliximab. Macrophages were infected with Escherichia coli, Enterococcus faecalis, Mycobacterium avium subsp. paratuberculosis (MAP) or M. avium subsp avium, and cytokine levels [tumour necrosis factor (TNF) and interleukin (IL)-10] were evaluated at different time-points. To evaluate infliximab-dependent effects on monocyte subsets, we studied CD14 and CD16 expression by peripheral blood monocytes before and after different infliximab administrations. We also investigated TNF secretion by macrophages obtained from CD16+ and CD16− monocytes and the frequency of TNF+ cells among CD16+ and CD16− monocyte-derived macrophages from CD patients. Infliximab treatment resulted in elevated TNF and IL-10 macrophage response to bacteria. An infliximab-dependent increase in the frequency of circulating CD16+ monocytes (particularly the CD14++CD16+ subset) was also observed (before infliximab: 4·65 ± 0·58%; after three administrations: 10·68 ± 2·23%). In response to MAP infection, macrophages obtained from CD16+ monocytes were higher TNF producers and CD16+ macrophages from infliximab-treated CD patients showed increased frequency of TNF+ cells. In conclusion, infliximab treatment increased the TNF production of CD macrophages in response to bacteria, which seemed to depend upon enrichment of CD16+ circulating monocytes, particularly of the CD14++CD16+ subset. Infliximab treatment of CD patients also resulted in increased macrophage IL-10 production in response to bacteria, suggesting an infliximab-induced shift to M2 macrophages.

Previous studies have shown that haemodialysis patients have an increased risk of trace element imbalances. Most studies have determined the concentration of trace elements in serum only, but most trace elements are not uniformly distributed between plasma and blood cells, which justifies separate analysis of the different compartments. In this study, we determined both the serum and whole blood concentration of a wide panel of trace elements (Li, B, Mn, Co, Ni, Cu, Zn, Se, Rb, Sr, Mo, Cd, Pb) in haemodialysis patients and compared them with those of a control group. Whole blood and serum samples were collected during routine laboratory testing of patients undergoing chronic haemodialysis. For comparison purposes, samples from individuals with normal renal function were also analysed. Statistically significant differences (p < 0.05) were found between the two groups for whole blood concentrations of all analysed elements except Zn (p = 0.347). For serum, the difference between groups was statistically significant for all elements (p < 0.05). This study confirms that patients on haemodialysis tend to present significant trace element imbalances. By determining the concentration of trace elements in both whole blood and serum, it was shown that chronic haemodialysis may affect intra- and extracellular blood compartments differently.

The objective of this study was to investigate the factors underlying the development of metabolic syndrome (MetS) in HIV-infected patients. Two hundred and sixty-six clinical cases were selected for a retrospective study. The sample was classified using the Adult Treatment Panel III guidelines and the identification of risk or protective factors associated with MetS evaluated via multivariate logistic or multinomial regressions. HIV-infected individuals diagnosed with MetS tend to be older, overweight, or obese (85% have a BMI ≥ 25), with a waist circumference > 90 cm (96.5 [88.8–105.5] cm, median [interquartile range]). Blood testing these individuals revealed high fasting levels of insulin (8.1 [5.8–21.6] pg/ml), glucose (98.0 [84.0–116.0] mg/dl), triglycerides (201.0 [142.0–267.3] mg/dl), and high-density lipoprotein cholesterol (36.5 [29.8–43.3] mg/dl) in addition with higher levels of inflammatory mediators such as high-sensitivity C-reactive protein (2.5 [1.0–4.9] mg/dl) and interleukin-6 (3.4 [2.8–3.8] pg/ml). The likelihood of HIV-infected individuals who are virally suppressed developing MetS is about 60% higher than those with acute infection. Treatment with nucleoside reverse transcriptase inhibitors (NRTIs) and protease inhibitors (PIs) increases the chance of developing MetS by around 2.4 times. Individuals with a lower antioxidant capacity (total antioxidant status [TAS] <1.33) have a 2.6 times higher risk of developing MetS. HIV-related chronic inflammation, a low TAS, and treatment with NRTIs in association with PIs are additional MetS risk factors.