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Clinical and Diagnostic Laboratory Immunology, March 1998, p. 211-218, Vol. 5, No. 2
1071-412X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Involvement of Antilipoarabinomannan Antibodies in Classical Complement Activation in Tuberculosis

Geir Hetland,1,* Harald G. Wiker,1 Kolbjørn Høgåsen,1 Beston Hamasur,2 Stefan B. Svenson,2 and Morten Harboe1

Institute of Immunology and Rheumatology, The National Hospital, Oslo, Norway,1 and Section of Bacteriology, Department of Veterinary Microbiology, University of Uppsala, Uppsala, Sweden2

Received 18 June 1997/Returned for modification 21 October 1997/Accepted 15 December 1997

We examined alternative and classical complement activation induced by whole bacilli of Mycobacterium bovis BCG and Mycobacterium tuberculosis products. After exposure to BCG, there were higher levels of the terminal complement complex in sera from Indian tuberculosis patients than in sera from healthy controls. The addition of BCG with or without EGTA to these sera indicated that approximately 70 to 85% of the total levels of the terminal complement complex was formed by classical activation. Sera from Indian tuberculosis patients contained more antibody to lipoarabinomannan (LAM) than sera from healthy Indians. Levels of anti-LAM immunoglobulin G2 (IgG2), but not anti-LAM IgM, correlated positively with classical activation induced by BCG in the sera. By flow cytometry, deposition of C3 and terminal complement complex on bacilli incubated with normal human serum was demonstrated. The anticomplement staining was significantly reduced in the presence of EGTA and EDTA. Flow cytometry also revealed the binding of complement to BCG incubated with rabbit anti-LAM and then with factor B-depleted serum. This indicates that classical activation plays a major role in complement activation induced by mycobacteria and that anti-LAM IgG on the bacilli can mediate this response. Classical complement activation may be important for the extent of phagocytosis of M. tuberculosis by mononuclear phagocytes, which may influence the course after infection.

* Corresponding author. Mailing address: Institute of Immunology and Rheumatology, The National Hospital, Fr. Qvamsgt. 1, N-0172 Oslo, Norway. Phone: 47 22 04 24 35. Fax: 47 22 35 36 05.

Clinical and Diagnostic Laboratory Immunology, March 1998, p. 211-218, Vol. 5, No. 2
1071-412X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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