Characterization of a Spontaneous Avirulent Mutant of Legionella pneumophila Serogroup 6: Evidence of DotA and Flagellin Involvement in the Loss of Virulence
Maria Scaturro1*, Stefania Meschini2, Giuseppe Arancia2, Fontana Stefano1, and Maria Luisa Ricci1
1Department of Infectious, Parasitic and Immune-Mediated Diseases, 2Department of Technology and Health, Istituto Superiore di Sanità, 00161-Rome, Italy
Journal of Microbiology, 47(6),768-773, 2009,
Legionella, pathogenesis, dotA, flagellin
The pathogenesis of Legionella pneumophila mainly resides in its ability to inhibit the phagosome-lysosome fusion, which normally prevents the killing of the host cells. In order to characterize the molecular alterations that occurred in a spontaneous avirulent mutant of Legionella pneumophila serogroup 6, named Vir-, we investigated the ability of the mutant to adhere to and multiply in the WI26VA4 alveolar epithelial cell line and in human macrophages, when compared to its parental strain, Vir+. We also determined the co- localization of bacteria with LAMP-1 to gain an insight into the phagosome-lysosome fusion process. Additionally, we determined the flagellin expression and dotA nucleotide sequencing. We observed a lack of expression of flagellin and an in-frame mutation in the dotA gene. The data obtained strongly suggest the loss of virulence of the mutant could probably be due to the absence of flagellin and the dysfunctional type IV secretion system, resulting from the DotA protein being severely compromised.