The common underlying host response in tuberculosis and other granulomatous repair processes is formation of granulomata. These granulomata include mononuclear phagocytes which originate from peripheral blood monocytes (MN). Since neutrophils precede monocytes at areas of granulomatous inflammation, we hypothesized that neutrophils initiate these inflammatory responses by releasing chemotaxins which attract monocytes. Our results supported this premise. First, neutrophils stimulated by tubercle bacilli released chemotactic factors for monocytes, both in vivo and in vitro. Second, in nitrogen mustard treated rabbits given BCG intrapleurally, neutropenia was associated with decreased numbers of macrophages, increased BCG colonies recoverable from pleural fluid, and decreased granuloma formation on pleural surfaces.
