Modulation of Host–Bacterial Interactions by Collectins

Pulmonary defenses against inhaled bacteria are complex, overlapping, and mechanistically heterogeneous. These include physical barriers and a diversity of biochemical and cellular defenses. Acquired humoral and cellular immunity are of obvious importance. However, innate, nonclonal mechanisms play important roles, particularly in the interval before the development of specific cellular immunity and in various immunodeficiency states. In the absence of specific immunity, innate mechanisms often determine whether bacterial inhalation is followed by immediate clearance, colonization with asymptomatic carriage, mucosal infection, tissue invasion, or dissemination and sepsis. In normal hosts and in the absence of exposure to unusually large numbers of virulent organisms, these natural frontline defenses appear sufficient to allow rapid bacterial clearance without the development of infection. Innate pulmonary immunity includes cell-mediated mechanisms that involve the activities of the resident and recruited phagocytes. In addition, there are a wide variety of constitutively or readily inducible proteins and peptides with antibacterial activities in vitro that accumulate in the lung in vivo. These substances are synthesized by epithelial cells, which line the airways and alveoli, and resident leukocytes. Putative pulmonary host-defense molecules include: