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lüll Pulmonary collectins in innate immunity of the lung Kuroki Y; Takahashi M; Nishitani CCell Microbiol 2007[Aug]; 9 (8): 1871-9Pulmonary collectins, hydrophilic surfactant proteins A and D (SP-A and SP-D), have been implicated in the regulation of pulmonary host defence and inflammation. SP-A and SP-D directly interact with a variety of microorganisms including bacteria and viruses, and attenuate the growth of Gram-negative bacteria, Histoplasma capsulatum and Mycoplasma pneumoniae. The collectins are thought to contribute to bacterial clearance. These lectins augment the phagocytosis of the bacteria by macrophages. SP-A serves as an opsonin and stimulates the uptake of bacteria and bacillus Calmette-Guerin through a C1q receptor- and an SP-R210-mediated processes. The collectin also stimulates FcR- and CR1-mediated phagocytosis by activating the macrophages. In addition, SP-A and SP-D directly interact with macrophages and enhance the phagocytosis of Streptococcus pneumoniae and Mycobacterium by increasing cell surface localization of the phagocytic receptors, scavenger receptor A and mannose receptor. The collectins also modulate pulmonary inflammation. SP-A and SP-D bind to cell surface receptors including Toll-like receptors, SIRPalpha and calreticulin/CD91, and attenuate or enhance inflammation in a microbial ligand-specific manner. In this article we review the immunomodulatory functions of SP-A and SP-D and their possible mechanisms in direct actions on microbes, macrophage phagocytosis and modulation of inflammation.|*Immunity, Innate[MESH]|Animals[MESH]|Collectins/*immunology[MESH]|Humans[MESH]|Lung/*immunology/microbiology[MESH]|Macrophages/immunology/microbiology[MESH]|Phagocytosis[MESH]|Pneumonia/*immunology/microbiology[MESH]|Pulmonary Surfactant-Associated Protein A/immunology[MESH]|Pulmonary Surfactant-Associated Protein D/immunology[MESH] |