Protective effect and mechanism of Schistosoma japonicum soluble egg antigen against type 1 diabetes in NOD mice

• Published in: International journal of diabetes in developing countries 2022-04, Vol.42 (2), p.363-368
• Main Authors: Wang, Li-xia, Gao, Yan-ru, Pan, Qun, Tang, Chun-lian, Zhang, Rong-hui, Li, Yan-hong, Zheng, Chun-lan
• Format: Article
• Language: English
• Subjects: Antigens; Cell culture; Diabetes; Diabetes mellitus (insulin dependent); Family Medicine; Flow cytometry; General Practice; Health Administration; Immune response (cell-mediated); Immunoregulation; Interleukin 4; Interleukin 5; Lymphocytes; Lymphocytes T; Medicine; Medicine & Public Health; Original Article; Schistosoma japonicum; Soluble egg antigen; Spleen; Splenocytes; γ-Interferon
• ISSN: 0973-3930; 1998-3832
• DOI: 10.1007/s13410-021-00970-4

Objective To study the effect and mechanism of Schistosoma japonicum soluble egg antigen (SEA) on protecting against type 1 diabetes, 4-week-old female BALB/c and NOD mice were divided randomly into four groups: BALB/c control, BALB/c treated with SEA, NOD control, and NOD treated with SEA. Methods Treated mice were injected intraperitoneally with 50 μg of SEA twice a week for 6 weeks, and control mice received the same volume of phosphate-buffered saline. Blood glucose in all mice was determined weekly from 8 weeks of age. Flow cytometry was used to detect the percentages of regulatory T cells of splenocytes in each group. Enzyme-linked immunosorbent assays were used to detect the levels of interferon-γ, interleukin (IL)-2, IL-4, and IL-5 in splenic cell culture supernatants. Results Compared with those of the NOD group, the blood glucose level and percentage incidence of diabetes in NOD mice treated with SEA decreased significantly. This indicated that SEA treatment prevented spontaneous type 1 diabetes. After SEA administration, the frequency of splenic regulatory T cells increased significantly, and the secretion of IL-4 and IL-5 by splenic cells increased. Conclusions These results demonstrated that SEA can prevent type 1 diabetes by enhancing regulatory T cells and the T helper 2 cell immune response in NOD mice.