Abstract
Cationic antimicrobial peptides (CAMP) form an important part of the innate immune response in many organisms ranging from humans to amoebae. The fact that CAMP resistance mechanisms exist in Legionella pneumophila is suggested by several lines of evidence. Investigations were undertaken to investigate the role of the pagP-like gene in L. pneumophila in CAMP resistance and intracellular infections. To investigate the role of the pagP-like gene in CAMP resistance, the MICs of PmB, a bacterially derived CAMP, and C18G, a synthetic CAMP based on human platelet activating factor IV, were assessed for the mutants generated. Consequently, bacterial growth in low Mg2+ minimal media increases the CAMP resistance generated by pagP. CAMP resistance to PmB or C18G was increased by growth in low-Mg2+ CDM in both 130b and NU260. Thus, there was no obvious defect in the initial stages of infection, i.e., attachment and invasion. Intracellular growth of both wild type and mutant was also tested in a coculture assay with Hartmannella vermiformis. This amoeba is known to support the growth of L. pneumophila and was isolated from a clinical case of legionellosis.
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