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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 ,
H. Bootsma ,
B. I. Mulder ,
C. G. M. Kallenberg  and
D. Van der Waaij
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
Information
Epidemiology & Infection , Volume 114 , Issue 1 , February 1995 , pp. 133 - 141
Copyright
Copyright © Cambridge University Press 1995

References

REFERENCES

1.Tan, EM. Autoantibodies to nuclear antigens (ANA): their immunobiology and medicine. Adv Immunol 1982; 33: 167–240.Google ScholarPubMed
2.Borg, EJ ter, Horst, G, Hummel, EJ, Limburg, PC, Kallenberg, CGM. Measurement of increases in anti-double-stranded DNA antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus. Arthritis Rheum 1990; 33: 634–43.CrossRefGoogle ScholarPubMed
3.Waaij, D van der. The composition of the microflora, functional aspects of the intestinal immune system and auto-immune phenomena. In Sazaki, S, ed. Recent advances in germfree research. Tokai: Tokai University Press 1981: 387–95.Google Scholar
4.Penhale, WJ, Young, PR. The influence of the normal microbial flora on the susceptibility of rats to experimental autoimmune thyroiditis. Clin Exp Immunol 1988; 72: 288–92.Google ScholarPubMed
5.Lieberum, B, Hartman, K. Successive changes of the cellular composition in lymphoid organs of MLR-MP/lpr-lpr mice during the development of lymphoproliferative disease as investigated in cryosections. Clin Immunol Immunopathol 1988; 46: 421–31.CrossRefGoogle Scholar
6.Klinman, DM. Regulation of B cell activation in autoimmune mice. Clin Immunol Immunopathol 1989; 53: S25–S34.CrossRefGoogle ScholarPubMed
7.Klinman, DM. Polyclonal B cell activation in lupus-prone mice precedes and predicts the development of autoimmune disease. J Clin Invest 1990; 86: 1249–54.CrossRefGoogle ScholarPubMed
8.Borg, EJ ter, Horst, G, Hummel, E., Limburg, PC, Kallenberg, CGM. Rises in anti-double stranded DNA antibody levels prior to exacerbations of systemic lupus erythematosus are not merely due to polyclonal B cell activation. Clin Immunol Immunopathol 1991; 59: 117–28.CrossRefGoogle Scholar
9.Carroll, P, Stafford, D, Schwartz, RS, Stollar, BD. Murine monoclonal anti-DNA autoantibodies bind to endogenous bacteria. J Immunol 1985; 135: 1086–90.CrossRefGoogle ScholarPubMed
10.Karounos, DG, Grudier, JP, Pisetsky, DS. Spontaneous expression of antibodies to DNA of various species origin in sera of normal subjects and patients with systemic lupus erythematosus. J Immunol 1988; 140: 451–5.CrossRefGoogle ScholarPubMed
11.Gilkeson, GS, Pritchard, AJ, Pisetsky, DS. Specificity of anti-DNA antibodies induced in normal mice by immunization with bacterial DNA. Clin Immunol Immunopathol 1991; 59: 288–300.CrossRefGoogle ScholarPubMed
12.Dziarski, R. Autoimmunity: polyclonal activation or antigen induction? Immunology Today 1988; 9: 340–2.CrossRefGoogle ScholarPubMed
13.Pisetsky, DS, Grudier, JP, Gilkeson, GS. A role for immunogenic DNA in the pathogenesis of systemic lupus erythematosus. Arthritis Rheum 1990; 33: 153–9.CrossRefGoogle ScholarPubMed
14.Terada, K, Okuhara, E, Kawarada, Y. Antigen DNA isolated from immune complexes in plasma of patients with systemic lupus erythematosus hybridizes with the Escherichia coli lac Z gene. Clin Exp Immunol 1991; 85: 66–9.CrossRefGoogle ScholarPubMed
15.Murosaki, S, Yoshikai, Y, Kubo, C et al. , Influence of intake of skim milk from cows immunized with intestinal bacterial antigens on onset of renal disease in (NZB + NZW)F1 mice fed ad libitum or restricted in energy intake. J Nutrition 1991; 121: 1860–8.CrossRefGoogle ScholarPubMed
16.Apperloo-Renkema, HZ, Wilkinson, MHF, Waaij, D van der. Circulating antibodies against faecal bacteria assessed by immunomorphometry: combining quantitative immunofluorescence and image analysis. Epidemiol Infect 1992; 109: 497–506.CrossRefGoogle ScholarPubMed
17.Liang, MH, Socher, SA, Larson, MG, Schur, PH. Reliability and validity of six systems for the clinical assessment of disease activity in systemic lupus erythematosus. Arthritis Rheum 1989; 32, 1107–18.CrossRefGoogle ScholarPubMed
18.Forrest, BD. Identification of an intestinal immune response using peripheral blood lymphocytes. Lancet 1988; i: 81–3.CrossRefGoogle Scholar
19.Swaak, AJG, Aarden, LA, Statius van Eps, LW, Feltkamp, TEW. Anti-dsDNA and complement profiles as prognostic guides in systemic lupus erythematosus. Arthritis Rheum 1979: 22: 226–35.CrossRefGoogle ScholarPubMed
20.Adib, M, Rigimbeau, J, Avrameas, S, Ternynck, T. IgG autoantibody activity in normal mouse serum is controlled by IgM. J Immunol 1990; 145: 3807–13.CrossRefGoogle ScholarPubMed