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Experimental IgA nephropathy induced by Haemophilus parainfluenzae antigens

IgA nephropathy(IgAN) was first reported by Berger in 1968, and characterized by diffuse IgA deposition in mesangium. Patients with IgAN have usually episodic macroscopic hematuria accompanied with pharingitis, gastroenteritis, bronchitis, or sinusitis. These findings suggest that IgAN is an immune-complex disease resulting from a poorly controlled mucosal immune response to environmental antigens to which the patients were chronically exposed. We reported glomerular deposition of outer membrane of Haemophilus parainfluenzae (OMHP) antigens and the presence of IgA antibody against OMHP in the sera of patients with IgAN. These suggest that Haemophilus parainfluenzae has a role in the etiology of this disease. Furthermore, Endo et al. reported experimental IgA nephropathy induced by Gram-negative bacteria. This study was conducted to determine whether intraperitoneal administration of OMHP antigens induced immunohistologically evident glomerular deposition of IgA and C3 in C3H/HeN mice. Female C3H/HeN mice (4 weeks old) were fed on commercial pellet mouse foods. The mice received intraperitoneal injection of OMHP antigens, once per week (OMHP group). The control group received intraperitoneal injection of PBS. The mice were killed at 10, 20 and 30 weeks after the experiment commenced. Throughout the experiments, hematuria and proteinuria were analyzed every 5 weeks. The OMHP group showed glomerular deposition of IgA, C3 and OMHP antigens, glomerular changes (mesangial hypercellularity and increase of mesangial matrix) at 20 and 30 weeks. The control group showed no glomerular deposition of IgA, C3 and OMHP antigens and no glomerular change. Hematuria was recognized in one of six OMHP group mice at 30 weeks. These results suggest that OMHP antigens play a role in the glomerular deposition of IgA and C3 in C3H/HeN mice. This is the first use of OMHP antigens to establish an active model of IgAN.