The Legionella pneumophila Collagen-Like Protein Mediates Sedimentation, Autoaggregation, and Pathogen-Phagocyte Interactions

Abstract

ABSTRACTAlthough only partially understood, multicellular behavior is relatively common in bacterial pathogens. Bacterial aggregates can resist various host defenses and colonize their environment more efficiently than planktonic cells. For the waterborne pathogenLegionella pneumophila, little is known about the roles of autoaggregation or the parameters which allow cell-cell interactions to occur. Here, we determined the endogenous and exogenous factors sufficient to allow autoaggregation to take place inL. pneumophila. We show that isolates fromLegionellaspecies which do not produce theLegionellacollagen-like protein (Lcl) are deficient in autoaggregation. Targeted deletion of the Lcl-encoding gene (lpg2644) and the addition of Lcl ligands impair the autoaggregation ofL. pneumophila. In addition, Lcl-induced autoaggregation requires divalent cations.Escherichia coliproducing surface-exposed Lcl is able to autoaggregate and shows increased biofilm production. We also demonstrate thatL. pneumophilainfection ofAcanthamoeba castellaniiandHartmanella vermiformisis potentiated under conditions which promote Lcl dependent autoaggregation. Overall, this study shows thatL. pneumophilais capable of autoaggregating in a process that is mediated by Lcl in a divalent-cation-dependent manner. It also reveals that Lcl potentiates the ability ofL. pneumophilato come in contact, attach, and infect amoebae.