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Host-microflora interaction in systemic lupus erythematosus (SLE): circulating antibodies to the indigenous bacteria of the intestinal tract

Published online by Cambridge University Press:  15 May 2009

H. Z. Apperloo-Renkema
Affiliation:
Laboratory for Medical Microbiology and State University Groningen, Groningen, The Netherlands
H. Bootsma
Affiliation:
Department of Clinical Immunology, State University Groningen, Groningen, The Netherlands
B. I. Mulder
Affiliation:
Laboratory for Medical Microbiology and State University Groningen, Groningen, The Netherlands
C. G. M. Kallenberg*
Affiliation:
Department of Clinical Immunology, State University Groningen, Groningen, The Netherlands
D. Van der Waaij
Affiliation:
Laboratory for Medical Microbiology and State University Groningen, Groningen, The Netherlands
*
C. G. M. Kallenberg, Department of Clinical Immunology, Oostersingel 59, 9713 EZ Groningen, The Netherlands.
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Experimental data suggest a role for the microflora in the disease expression of systemic lupus erythematosus (SLE). In active SLE anti-ds-DNA antibodies are supposed to be pathogenic by forming immune complexes with DNA. Bacteria might induce the production of anti-ds-DNA antibodies. To explore the relation between the host and his microflora in SLE in comparison with healthy controls we studied the prevalence of systemic antibodies to faecal bacteria that were discriminated by their morphology by indirect immunofluorescence.

IgM titres against their own faecal microflora were found to be lower both in active and inactive SLE when compared to healthy individuals. IgG-class antibacterial antibodies were increased in inactive SLE but decreased in active SLE compared to inactive SLE and healthy controls, although plasma levels of total IgG were almost doubled in active SLE. The lower IgG antibacterial antibody titres in active SLE might possibly result from sequestration of these IgG antibodies in immune complexes, indicating a possible role for antibacterial antibodies in exacerbations of SLE.

Type
Special Article
Copyright
Copyright © Cambridge University Press 1995

References

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