Macrophage inflammatory proteins MIP-1 and MIP-2 are involved in T cell-mediated neutrophil recruitment

Abstract

Mice intraperitoneally (i.p.) infected with Mycobacterium bovis bacille Calmette-Guérin (BCG) respond to an i.p. challenge with mycobacterial antigen with an acute and extensive accumulation of neutrophils. This influx was not mimicked by the inoculation of recombinant interferon-gamma (IFN-gamma) or tumor necrosis factor alpha (TNF-alpha). The antigen-induced recruitment of neutrophils was not affected by coinoculation of anti-IFN-gamma antibodies, was enhanced by anti-TNF-alpha antisera, and was significantly reduced by antisera against macrophage inflammatory proteins MIP-1 and MIP-2. The latter two sera had no additive effects. We hypothesize that mycobacteria-specific T cells are triggered by antigen to secrete MIP-1 and MIP-2, which directly mediate, at least partly, the influx of neutrophils that takes place in this model.