Mast cells display a distinct spatial distribution in the lung where they are found preferentially in intraepithelial locations or in deeper tissue around blood vessels, bronchioles and mucus secreting glands. Yet the physiological role of these granule-laden cells is unknown. There are now intriguing signs that their distinctive distribution together with their intrinsic capacity to release large amounts of inflammatory mediators serve a critical role in immune surveillance. Mast cells have now been shown to be capable of recognizing and aggressively reacting to a wide range of bacteria. The mast cell responses involve ingesting and killing of adherent bacteria, in a manner not unlike that of traditional phagocytic cells. Concomitant with this endocytic activity, a large variety of potent inflammatory mediators are released by the mast cell. One such mast cell-derived mediator, TNF-alpha, was recently shown to be a critical signal for initiating neutrophil influx to sites of bacterial infection in the lung as well as the peritoneum of mice. This capacity of mast cells to recruit neutrophils, together with its recently reported participation in processing and presenting bacterial antigens to immune cells and in mediating proliferation of epithelial cells and mucosal mucus secretion, indicate that mast cells have an extraordinary ability to modulate the innate as well as adaptive immune responses to infectious microorganisms.