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IL-33 is a recently identified cytokine, encoded by the IL-33 gene, which is a member of the IL-1 family that drives the production of T-helper-2 (Th-2)-associated cytokines. Serum levels of IL-33 have been reported to be up-regulated in various T-helper (Th)-1/Th-17-mediated diseases, such as psoriasis, rheumatoid arthritis, and inflammatory bowel. To investigate whether cytokine imbalance plays a role in the pathogenesis of vitiligo, we performed a case-control association study by enzyme-linked immunosorbent assay of IL-33 in our patients. IL-33 serum levels were measured by a quantitative enzyme immunoassay technique in patients with non-segmental generalized vitiligo and compared with those of healthy controls. IL-33 serum levels in patients with vitiligo were significantly increased than those in healthy controls. There was a positive correlation of IL-33 serum levels with extension of vitiligo and disease activity. This study suggests a possible systemic role of IL-33 in the pathogenesis of vitiligo. Inhibiting IL-33 activity might be a novel therapeutic strategy in the treatment of autoimmune inflammatory disease, like vitiligo. [ABSTRACT FROM AUTHOR]

Evidence shows that tobacco smoking interacts with development of rheumatic diseases. Increase in white cells count (leukocytosis) is frequently present, and in smokers, it is considered a biomarker of cardiovascular risk. Aim of the study is to evaluate this biomarker in smokers with rheumatic diagnosis. We carried out an observational study on 115 rheumatic outpatients (26 men and 89 women) divided into two groups according to their smoking habit: one composed of 56 smokers, the other of 59 not smokers. Diagnosis and common routinary clinical parameters were collected. In the total sample, smokers were 48.69%. Most common diagnosis was osteoarthritis (OA) (40.87% of the total); smokers in OA women were 36.11%, smokers in OA men were 54.55%. Second most common diagnosis was rheumatoid arthritis (RA) (23.48% of the total); smokers in RA women were 40.91%; smokers in RA men were 80%. OA smokers showed a significant increase ( P < 0.05) in white cells count when compared with OA not smokers. Between RA smokers and not smokers, any clinical difference was found. RA subjects following regular pharmacological treatment in the last 2 months were 84.61%. OA patients treated with drugs in the last 2 months were only 22.2%. Results seem to confirm that smoking habit may influence the development as well as gender distribution of rheumatic diseases. They show also that in absence of pharmacological treatment in smokers affected by OA leukocytosis (biomarker of cardiovascular risk) is observed. [ABSTRACT FROM AUTHOR]

Rationale. Hypericum perforatum is used as a natural antidepressant, and other antidepressants have been marketed to aid in smoking cessation. Objective. We investigated the effects of an extract of Hypericum perforatum (Ph-50) on withdrawal signs produced by nicotine abstinence in mice. Methods. Nicotine (2 mg/kg, four injections daily) was administered for 14 days to mice. Different doses of Ph-50 (125–500 mg/kg) were administered orally immediately after the last nicotine injection. In another experiment, Ph-50 (500 mg/kg) was orally administered in combination with nicotine, i) starting from day 8 until the end of the nicotine treatment period, or ii) during nicotine treatment and after nicotine withdrawal, or iii) immediately after the last nicotine injection. On withdrawal from nicotine, all animals were evaluated for locomotor activity and abstinence signs. Results. The locomotor activity reduction induced by nicotine withdrawal was abolished by Ph-50, which also significantly and dose-dependently reduced the total nicotine abstinence score when injected after nicotine withdrawal. Conclusions. These data show that treatment with Hypericum perforatum attenuates nicotine withdrawal signs in mice. Further studies are necessary to test the possibility that it may be used for smoking cessation treatment in humans. [ABSTRACT FROM AUTHOR]