Oral administration of lipopolysaccharides activates B-1 cells in the peritoneal cavity and lamina propria of the gut and induces autoimmune symptoms in an autoantibody transgenic mouse

• Published in: The Journal of experimental medicine 1994-07, Vol.180 (1), p.111-121
• Main Authors: MURAKAMI, M, TSUBATA, T, SHINKURA, R, NISITANI, S, OKAMOTO, M, YOSHIOKA, H, USUI, T, MIYAWAKI, S, HONJO, T
• Format: Article
• Language: English
• Subjects: Administration, Oral; Animals; Autoantibodies - genetics; Autoantibodies - physiology; Autoimmune Diseases - etiology; Autoimmunity (experimental aspects and models); B-Lymphocytes - immunology; Bacterial Infections - complications; Biological and medical sciences; Clonal Deletion; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Intestines - immunology; Lipopolysaccharides - administration & dosage; Lipopolysaccharides - pharmacology; Lymphocyte Activation; Male; Mice; Mice, Transgenic; Peritoneal Cavity - cytology
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.180.1.111

About a half of the antierythrocyte autoantibody transgenic (autoAb Tg) mice, in which almost all B cells are detected in the spleen, lymph nodes, and Peyer's patches, but not in the peritoneal cavity, suffer from autoimmune hemolytic anemia. The occurrence of this disease is strongly linked to production of autoAb by activated peritoneal B-1 cells in the Tg mice. In this study, we have shown that oral administration of lipopolysaccharides (LPS) activated B-1 cells in the lamina propria of the gut as well as the peritoneal cavity in the healthy Tg mice and induced the autoimmune symptoms in all the Tg mice. The activation of peritoneal and lamina propria B-1 cells by enteric LPS is found not only in the anti-RBC autoAb Tg mice and normal mice but also in the aly mice which congenitally lack lymph nodes and Peyer's patches. These results suggest that B-1 cells in the two locations may form a common pool independent of Peyer's patches and lymph nodes, and can be activated by enteric thymus-independent antigens or polyclonal activators such as LPS. The induction of autoimmune hemolytic anemia in the Tg mice by enteric LPS through the activation of B-1 cells in the lamina propria of gut and in the peritoneal cavity suggests that B-1 cells and bacterial infection may play a pathogenic role in the onset of autoimmune diseases.