AI Article Synopsis

  • Evidence indicates that patients with IgA nephropathy (IgAN) have increased IgA production, potentially linked to the presence of Haemophilus parainfluenzae in the tonsils.
  • A study compared interferon-gamma (IFN-gamma) and IgA production from tonsillar mononuclear cells (TMC) in IgAN patients versus those with chronic tonsillitis (CT) after tonsillectomies.
  • Results showed that IgAN patients had higher spontaneous IFN-gamma and total IgA production, and while stimulation with outer membranes of HP increased HP-specific IgA in IgAN, it did not affect IFN-gamma levels, suggesting a complex relationship in the disease's development.

Article Abstract

Much evidence, both in vivo and in vitro, suggests that patients with IgA nephropathy (IgAN) have enhanced IgA production. We hypothesized that Haemophilus parainfluenzae (HP) in the tonsil plays an important role in the IgA production of IgAN patients. In this study, we focused on interferon-gamma (IFN-gamma) and IgA production by tonsillar mononuclear cells (TMC) in patients with IgAN. Tonsillectomies were performed in patients with IgAN and chronic tonsillitis (CT). The induction of IFN-gamma and IgA in vitro by TMC from IgAN patients was compared with that from CT patients. In addition, we investigated whether stimulation with the outer membranes of HP (OMHP) enhanced IFN-gamma and IgA induction by TMC from patients with IgAN. Spontaneous IFN-gamma production and spontaneous total IgA production by TMC were higher in IgAN patients than in those patients with CT (p < 0.05). IFN-gamma induction by OMHP stimulation was also higher in IgAN patients than in CT patients. The stimulation of OMHP enhanced HP-specific IgA in IgAN but had no influence on the production of IFN-gamma in patients with either IgAN or CT compared with spontaneous IFN-gamma production. IFN-gamma production was positively correlated with total IgA values in both IgAN and CT patients, but not with HP-specific IgA. These results suggest that increased IFN-gamma production in patients with IgAN is not associated with HP infection but may play a role in the pathogenesis of IgAN.

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http://dx.doi.org/10.1080/000164800750000496DOI Listing

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