Am. J. Respir. Crit. Care Med., Volume 162, Number 2, August 2000, 486-489

Mycobacterial Lipoarabinomannan Induces an Inflammatory Response in the Mouse Lung
A Role for Interleukin-1

NICOLE P. JUFFERMANS, ANNELIES VERBON, JOHN T. BELISLE, PRESTON J. HILL, PETER SPEELMAN, SANDER J. H. van DEVENTER, and TOM van der POLL

Laboratory of Experimental Internal Medicine, Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and Department of Microbiology, Colorado State University, Fort Collins, Colorado

Lipoarabinomannan (LAM), a cell wall component of Mycobacterium tuberculosis, induces the production of cytokines and chemokines in vitro. Interleukin-1 (IL-1) contributes to granuloma formation in tuberculosis (TB), and exerts effects via the IL-1 receptor type I (IL-1R). To determine the effects of LAM in the pulmonary compartment in vivo and to establish the role of endogenous IL-1 herein, normal and IL-1R deficient (^/) mice were intranasally inoculated with LAM (50 µg). In normal mice, LAM resulted in a neutrophilic cell influx into the bronchoalveolar lavage fluid (BALF). LAM also induced increases in the lung concentrations of macrophage inflammatory protein-2 (MIP-2), keratinocyte (KC), tumor necrosis factor- (TNF-), IL-1, and IL-1. IL-1R^/ mice had less influx of granulocytes in their BALF than wild-type mice. Also, lung TNF- levels were lower in IL-1R^/ mice. LAM may be an important stimulator of innate immunity in infection with M. tuberculosis via mechanisms that involve endogenous IL-1 activity.

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