Epidemiology of urticaria in China: a population-based study.

BACKGROUND: Urticaria is a common skin disease characterized by episodes of wheals, and it has a negative effect on patients' quality of life. Large-scale population-based epidemiological studies of urticaria are scarce in China. The aim of this survey was to determine the prevalence, clinical forms, and risk factors of urticaria in the Chinese population. METHODS: This survey was conducted in 35 cities from 31 provinces, autonomous regions, and municipalities of China. Two to three communities in each city were selected in this investigation. Participants completed questionnaires and received dermatological examinations. We analyzed the prevalence, clinical forms, and risk factors of urticaria. RESULTS: In total, 44,875 questionnaires were distributed and 41,041 valid questionnaires were collected (17,563 male and 23,478 female participants). The lifetime prevalence of urticaria was 7.30%, with 8.26% in female and 6.34% in male individuals ( P  < 0.05). The point prevalence of urticaria was 0.75%, with 0.79% in female and 0.71% in male individuals ( P  < 0.05). Concomitant angioedema was found in 6.16% of patients. Adults had a higher prevalence of urticaria than adolescents and children. Living in urban areas, exposure to pollutants, an anxious or depressed psychological status, a personal and family history of allergy, thyroid diseases, and Helicobacter pylori infection were associated with a higher prevalence of urticaria. Smoking was correlated with a reduced risk of urticaria. CONCLUSION: This study demonstrated that the lifetime prevalence of urticaria was 7.30% and the point prevalence was 0.75% in the Chinese population; women had a higher prevalence of urticaria than men. Various factors were correlated with urticaria.

Effects of tumor necrosis factor-like ligand 1A (TL1A) on imiquimod-induced psoriasiform skin inflammation in mice.

TL1A, as a master regulatory cytokine, plays a key role in the development of diverse T-cell-mediated inflammatory and autoimmune diseases. Our study is to further understand the roles of TL1A in the pathogenic mechanism of psoriasis and to find a possible new therapeutic strategy in the treatment of psoriasis. The direct effects of TL1A injection in mice skin and the therapeutic effects of TL1A blockade in imiquimod (IMQ)-induced psoriasis-like mouse model were researched in this study. First, we found that the expressions of TL1A in IMQ-treated lesions were significantly higher than Vaseline control group. And then, the results showed that TL1A injection exacerbated the psoriasiform phenotype on IMQ-treated skin (including clinical score, epidermal thickness changes, and Baker score) by increasing the number of T cells, neutrophils, and DCs, and upregulating the mRNA expression of IFN-γ and IL-17. However, anti-TL1A mAb can alleviate psoriasis-like lesions in clinical and effectively improved the histopathologic changes in IMQ-induced psoriasis-like mice after treatment. Moreover, anti-TL1A mAb also reduced the number of infiltrated CD3+ T cells, MPO+ neutrophils, and CD11c+ DCs in psoriasis-like lesions, and obviously decreased the expression of IFN-γ and IL-17 in psoriasis-like lesions. Data suggested that TL1A might be involved in the pathogenesis of psoriasis, and targeting TL1A by anti-TL1A mAb might provide a solid foundation and novel therapeutic sight in the treatment of psoriasis.

Expression of death receptor 3 (DR3) on peripheral blood mononuclear cells of patients with psoriasis vulgaris.

BACKGROUND: A series of previous reports indicated that tumour necrosis factor-like ligand 1A (TL1A) and its receptor death receptor 3 (DR3) are involved in the pathogenesis of psoriasis vulgaris (PV), which is a common chronic skin disease accompanied by a number of comorbidities, although their exact roles remain unclear. Our previous studies demonstrated that serum TL1A levels were substantially elevated in patients with PV, but the detection of DR3 expression in peripheral blood mononuclear cells (PBMCs) of patients with PV had not been reported. Therefore, we detected DR3 expression on CD4+, CD8+, CD14+ and CD19+ PBMCs of patients with PV, atopic dermatitis (AD) and healthy volunteers. METHODS: Blood samples were collected from participants with PV before and after treatment. Then, PBMCs from patients with PV were isolated. The Psoriasis Area Severity Index (PASI) was used to assess severity in patients with PV. The DR3 on CD4+, CD8+, CD14+ and CD19+ PBMCs were detected by flow cytometry analysis. Pearson's correlation analysis was then used to investigate the relationship between DR3 expression and PASI scores in patients with PV. RESULTS: Comparing with the healthy volunteers and patients with AD, the percentage of DR3-expressing on CD8+ and CD14+ PBMCs in patients with PV was elevated, but the percentage of DR3-expressing on CD8+ and CD14+ cells decreased after anti-inflammatory treatment, which was correlated with PASI scores. CONCLUSIONS: Taken together, these findings suggest that DR3 may play a key role in the pathogenesis of PV.