IgA nephropathy (IgAN) was first reported by Berger in 1968, and characterized by diffuse
IgA deposition in the mesangium. Patients with IgAN have usually episodic macroscopic
hematuria accompanied with
pharyngitis,
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 patient was chronically exposed. We reported the glomerular deposition of the 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 plays a role in the aetiology of this disease. This study was conducted to determine whether OMHP
antigens induced immunohistologically evident glomerular deposition of
IgA and C3 in C3H/HeN mice. Female C3H/HeN mice (4 weeks old) received
intraperitoneal injection (HP-IP group), and
oral administration (HP-PO group) of OMHP
antigens. The control group similarly received
intraperitoneal injection of PBS, and oral intake of ordinary water. The mice were sacrificed
at 10, 20, 30, 40, 50 weeks after the start of the experiment. The HP-IP group showed glomerular deposition of
IgA, C3 and OMHP
antigens, glomerular changes (Mesangial hypercellularity and increase in mesangial matrix) after 20 weeks. The HP-PO group showed only mild deposition of
IgA, and mild increase in mesangial matrix. 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.