1995 Fiscal Year Final Research Report Summary
Study of Haemophilus parainfluenzae antigen and antibody in the etiology of IgA nephropathy
| Project/Area Number |
06671135
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | Fukui Medical School (1995)
Niigata University (1994) |
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Principal Investigator |
SUZUKI Satoru Fukui Medical School, Assistant professor, 医学部, 助教授 (00206484)
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| Project Period (FY) |
1994 – 1995
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| Keywords | IgA nephropathy / Haemophilus parainfluenzae / Haemophilus influenzae / Amino acid sequence / Outer membrane |
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| Research Abstract |
We previously demonstrated a close relationship between the outer membranes of Haemophilus parainfluenzae (HP) antigens (OMHP) and IgA nephropathy. Our objective was to clarify the relationship among IgA-, IgG-, and IgM-class antibody (Ab) against OMHP in the sera of 44 patients with IgA nephropathy and 62 patients with other glomerular diseases (OGD) by enzyme-linked immunosorbent assay (ELISA). Patients with IgA nephropathy showed a significantly higher level of IgA-Ab (P<0.0005) and IgG-Ab (P<0.001) against OMHP,than did patients with OGD.Positive correlations were observed between IgA-and IgG-Ab, between IgA-and IgM-Ab, and between IgG-and IgM-Ab against OMHP in the sera of patients with IgA nephropathy. Immunoblotting showed that IgA-, IgG-, or IgM-Ab against OMHP in the sere of all patients with IgA nephropathy bound to the components of OMHP.Amino acid sequences of three components of OMHP recognized by the sera from patients with IgA nephropathy revealed the homology with those reported for outer membrane protein (OMP) P6 precursor, OMP P5, and P2 porin protein of Haemophilus influenzae.
Results suggest that patients with IgA nephropathy have glomerular deposits of OMP P6 precursor, OMP P5, or P2 porin protein of HP,and a specific increase in the production of IgA-Ab against OMHP via polyclonal activation against these, with switching of production from one isotype to another, eg, from IgM to IgA.
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