title: Staphylococcus aureus antigens induce IgA-type glomerulonephritis in Balb/c mice.
abstract: BACKGROUND
  Staphylococcus aureus (S. aureus) is a common, normal pathogenic flora that colonizes mucosal tissues. We previously reported that glomerulonephritis occurs during methicillin-resistant S. aureus infection, and demonstrated polyclonal elevation of serum immunoglobulin A (IgA) and IgG levels and various histological findings, such as mesangial extracapillary and endocapillary proliferation. To investigate the pathogenic roles of S. aureus antigens, we induced IgA-type glomerulonephritis in mice by immunization with antigens derived from S. aureus, as a model of human IgA nephropathy (IgAN).
  
  
  METHODS
  Balb/c mice (Th2 dominant type) and C57BL/6 mice (Th1 dominant type) were immunized biweekly for 4 months with antigens derived from S. aureus mixed with Freund's incomplete adjuvant.
  
  
  RESULTS
  Mesangial proliferative glomerulonephritis with IgA, IgG and complement 3 (C3) depositions were observed in all Balb/c mice. Although C3 depositions and cell proliferation in the mesangial area were also seen in C57BL/6 mice, they were not correlated with urinary findings. In Balb/c mice, S. aureus antigens were detected in glomeruli using affinity-purified human anti-S. aureus antibodies, but there was no staining in C57BL/6 mice. The antibodies reacted with several S. aureus antigens, based on Western blot analysis, and the main 30-35 kDa band differed in intensity in Balb/c and C57BL/6 mice. In addition, increased transforming growth factor beta (TGF-beta) messenger RNA (mRNA) expression was seen in Balb/c mice compared to C57BL/6 mice.
  
  
  CONCLUSIONS
  S. aureus antigens including, in particular, a 30-35 kDa protein and the host genetic background could play important roles in IgA-like glomerulonephritis pathogenesis.
authors.affiliation: Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
authors.forename: Samina
authors.initials: S
authors.lastname: Sharmin
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Shimizu
authors.forename: Masahiro
authors.initials: M
authors.lastname: Hagiwara
authors.forename: Kouichi
authors.initials: K
authors.lastname: Hirayama
authors.forename: Akio
authors.initials: A
authors.lastname: Koyama
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology / Q000378:metabolism*; D001483:Base Sequence; D001707:Biopsy, Needle; D015153:Blotting, Western; D016207:Cytokines / Q000032:analysis*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005922:Glomerulonephritis, IGA / Q000276:immunology* / Q000473:pathology*; D007150:Immunohistochemistry; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D013211:Staphylococcus aureus / Q000276:immunology*; D016482:Urinalysis
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines