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Legionella pneumophila , the causative agent of Legionnaire's disease, replicates in human alveolar macrophages to establish infection. There is no human-to-human transmission and the main source of infection is  L. pneumophila  biofilms established in air conditioners, water fountains, and hospital equipments. The biofilm structure provides protection to the organism from disinfectants and antibacterial agents.  L. pneumophila  infection in humans is characterized by a subtle initial immune response, giving time for the organism to establish infection before the patient succumbs to pneumonia. Planktonic  L. pneumophila  elicits a strong immune response in murine, but not in human macrophages enabling control of the infection. Interactions between planktonic  L. pneumophila  and murine or human macrophages have been studied for years, yet the interface between biofilm-derived  L. pneumophila  and macrophages has not been explored. Here, we demonstrate that biofilm-derived  L. pneumophila  replicates significantly more in murine macrophages than planktonic bacteria. In contrast to planktonic  L. pneumophila , biofilm-derived  L. pneumophila  lacks flagellin expression, do not activate caspase-1 or -7 and trigger less cell death. In addition, while planktonic  L. pneumophila  is promptly delivered to lysosomes for degradation, most biofilm-derived bacteria were enclosed in a vacuole that did not fuse with lysosomes in murine macrophages. This study advances our understanding of the innate immune response to biofilm-derived  L. pneumophila  and closely reproduces the natural mode of infection in human.

Biofilm-derived Legionella pneumophila evades the innate immune response in macrophages