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lüll Phagocyte-bacteria interactions Keisari Y; Kabha K; Nissimov L; Schlepper-Schafer J; Ofek IAdv Dent Res 1997[Apr]; 11 (1): 43-9Recognition and phagocytosis of micro-organisms in a serum-poor environment represent innate immunity against many extracellular pathogens. As a paradigm for such processes, we discuss the recognition of Klebsiella pneumoniae by alveolar macrophages and monocyte-derived macrophages in the absence of serum. Macrophages recognize and subsequently kill Klebsiella expressing Man-alpha 2/3-Man or Rha-alpha 2/3-Rha sequences in their capsular polysaccharides by two mechanisms: (a) recognition of the capsular structures by macrophage mannose receptors, and (b) opsonization by the lung surfactant protein A (SP-A), which binds to the capsular polysaccharides of Klebsiella and to SP-A receptors on the macrophages. Sp-A may also enhance phagocytosis by increasing the activity of macrophage mannose receptors. We conclude that a specific microbial surface structure may be a target for recognition by macrophages via several mechanisms, as exemplified in the case of Klebsiella capsular polysaccharides. Multiple recognition mechanisms of pathogens by macrophages may be essential to provide innate immunity to reduce the frequency of infections caused by a relatively less virulent bacterium in the immuno-compromised host.|*Lectins, C-Type[MESH]|*Mannose-Binding Lectins[MESH]|*Pulmonary Surfactants[MESH]|Animals[MESH]|Candida albicans/metabolism/pathogenicity[MESH]|Humans[MESH]|Klebsiella Infections/etiology[MESH]|Klebsiella pneumoniae/*immunology/metabolism/pathogenicity[MESH]|Macrophages, Alveolar/physiology[MESH]|Macrophages/*physiology[MESH]|Mannose Receptor[MESH]|Opportunistic Infections/etiology[MESH]|Phagocytosis/*physiology[MESH]|Pneumonia, Bacterial/etiology[MESH]|Proteolipids/*physiology[MESH]|Pulmonary Surfactant-Associated Protein A[MESH]|Pulmonary Surfactant-Associated Proteins/*physiology[MESH]|Receptors, Cell Surface/metabolism/*physiology[MESH]|Virulence[MESH] |