Abstract: Kang Erxun*, Chen Hongquan, Yan Liping, Li Jie, Han Chunyu, Xia Xiujuan. *Department of Dermatology, Yantai Yuhuangding Hospital Affiliated to Medical College of Qingdao University, Yantai 264000, Shandong, China Corresponding author: Kang Erxun, Email: kangerxun2000@163.com 【Abstract】 Objective To investigate the relationship between anti-Helicobacter pylori （Hp） antibodies and development of chronic urticaria （CU）. Methods Fifty CU patients with positive 13C-urea breath test and anti-Hp antibodies, as well as 50 healthy human controls were recruited in this study. Serum samples were collected from all the subjects. The samples from the patients were subjected to tests for anti-high affinity IgE receptor （anti-FcεRI） and -IgE antibodies. Human mast cells （HMCs） were classified into several parts to be incubated with the sera of patients with CU, the sera of healthy controls with anti-IgE and -FcεRI antibodies respectively for 20 minutes. Those incubated with the sera of healthy controls without these antibodies served as the control. Subsequently, the levels of histamine released by HMCs were measured by enzyme-linked immunosorbent assay （ELISA）. Results The sera of CU patients showed a stronger ability to activate HMCs to release histamine than those of healthy controls （ （3.13 ± 0.93） μg/L vs （2.92 ± 0.75） μg/L, t = 2.39, P < 0.05）. Anti-FcεRI antibodies were detected in 4 patients, and anti-IgE antibodies in 3 patients. A significant increase was observed in the levels of histamine released by HMCs incubated with anti-FcεRI antibody-positive and anti-IgE antibody-positive patient-derived sera （t = 4.82, 6.34, respectively, both P < 0.01）, but not in those incubated with patient-derived sera only positive for anti-Hp antibodies （t = 1.74, P > 0.05） compared with those incubated with healthy control-derived sera. In comparison with the antibody-free healthy control-derived sera, those with anti-Hp IgG antibodies showed no significant effect on the release of histamines by HMCs （t = 1.95, P > 0.05）, whereas those with anti-FcεRI antibodies and anti-IgE antibodies exhibited an obvious promoting effect （t = 3.72, 3.02, respectively, both P < 0.01）. Conclusions The anti-Hp antibodies appears to have no role in the pathogenesis of CU, but the presence of anti-FcεRI and anti-IgE antibodies may contribute to the initiation of CU in patients with Hp infection.

Key words: Urticaria, Helicobacter pylori, Antibody, Mast cells