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Infection and Immunity, January 2000, p. 335-341, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Clearance and Organ Distribution of Mycobacterium tuberculosis Lipoarabinomannan (LAM) in the Presence and Absence of LAM-Binding Immunoglobulin M

Aharona Glatman-Freedman,1,2,3,* Aron J. Mednick,4 Nikoletta Lendvai,4 and Arturo Casadevall1,4,5

Division of Infectious Diseases,1 Departments of Pediatrics,2 Internal Medicine,5 and Microbiology and Immunology,4 and Children's Hospital at Montefiore,3 Albert Einstein College of Medicine, Bronx, New York 10461

Received 5 May 1999/Returned for modification 24 June 1999/Accepted 5 October 1999

Lipoarabinomannan (LAM) is a component of the mycobacterial surface which has been associated with a variety of deleterious effects on immune system function. Despite the importance of LAM to the pathogenesis of mycobacterial infection, there is no information available on its fate in vivo. In this study, we determined the pharmacokinetics and tissue distribution of exogenously administered LAM in mice. For measurements of serum and tissue LAM concentrations, we developed an enzyme-linked immunosorbent assay which used monoclonal antibodies of different isotypes to capture and detect LAM at concentrations of >= 0.4 µg/ml. Intravenous administration of LAM to mice resulted in transient serum levels with organ deposition in the spleen and in the liver. Immunohistochemical studies localized LAM to the spleen marginal zone macrophages and, to a lesser degree, to liver macrophages. When LAM was administered to mice previously given a LAM-binding immunoglobulin M (IgM), LAM was very rapidly cleared from circulation. In those mice, deposition of LAM in the spleen was significantly reduced while LAM deposition in the liver increased. Administration of LAM-binding IgM resulted in significant levels of IgM to LAM in bile consistent with an increased hepatobiliary excretion of LAM in the presence of specific antibody. Bile, liver extracts, and bile salts were found to rapidly inactivate the immunoreactivity of LAM. The results indicate that serum clearance and organ deposition of LAM in mice are affected by the presence of LAM-binding antibody and suggest a mechanism by which antibody could modify the course of mycobacterial infection.

* Corresponding author. Mailing address: Albert Einstein College of Medicine, Golding Building, Room 702, 1300 Morris Park Ave., Bronx, NY 10461. Phone: (718) 430-3768. Fax: (718) 430-8701. E-mail: afreedma{at}aecom.yu.edu.

Infection and Immunity, January 2000, p. 335-341, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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