Lectinophagocytosis mediated by bacterial surface lectins.

The evidence showing that non-opsonic recognition of bacteria by phagocytes involve interaction between bacterial surface lectin and sugars on the phagocytic cells is summarized. This process, termed lectinophagocytosis, probably occur in vivo as evident from experimental infections with mixed phenotypes one of which express mannose specific (MS) lectin which mediate lectinophagocytosis of the bacteria and the other does not. In all cases studied, the lectin bearing phenotype survived better in phagocytes-poor sites and the phenotype which does not express this lectin survived better in phagocytes-rich sites. Due to the phase variation phenomenon, an off-on switch allowing the bacterial clone to alternate between lectin expressing and non-expressing phenotypes, the invading bacteria grow as a mixture of phenotypes. The phenotype expressing fimbrial lectin for which receptors are accessible on phagocytic cells undergo lectinophagocytosis. The phenotypes not expressing fimbrial lectin or expressing lectin for which receptors are not available on phagocytic cells may escape phagocytosis and proliferate. It is postulated that pathogenesis of inflammation and tissue damage following infections with MS lectin bearing bacteria may be partly due to both bacterial proliferation resulting in the release of toxic products and to lectinophagocytosis associated with the release of inflammatory agents.