| Staphylococcus aureus antigens induce IgA-type glomerulonephritis in Balb/c mice. | |
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MedLine Citation:
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PMID: 15372411 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Samina Sharmin; Yoshio Shimizu; Masahiro Hagiwara; Kouichi Hirayama; Akio Koyama |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of nephrology Volume: 17 ISSN: 1121-8428 ISO Abbreviation: J. Nephrol. Publication Date: 2004 Jul-Aug |
Date Detail:
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Created Date: 2004-09-16 Completed Date: 2004-12-23 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9012268 Medline TA: J Nephrol Country: Italy |
Other Details:
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Languages: eng Pagination: 504-11 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Antigens, Bacterial / immunology, metabolism* Base Sequence Biopsy, Needle Blotting, Western Cytokines / analysis* Disease Models, Animal Enzyme-Linked Immunosorbent Assay Glomerulonephritis, IGA / immunology*, pathology* Immunohistochemistry Mice Mice, Inbred BALB C Mice, Inbred C57BL Molecular Sequence Data Reverse Transcriptase Polymerase Chain Reaction Sensitivity and Specificity Staphylococcus aureus / immunology* Urinalysis |
| Chemical | |
Reg. No./Substance:
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0/Antigens, Bacterial; 0/Cytokines |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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