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The human pathogen  Legionella pneumophila  must evade host cell death signaling to enable replication in lung macrophages and to cause disease. After bacterial growth, however,  L. pneumophila  is thought to induce apoptosis during egress from macrophages. The bacterial effector protein, SidF, has been shown to control host cell survival and death by inhibiting pro-apoptotic BNIP3 and BCL-RAMBO signaling. Using live-cell imaging to follow the  L. pneumophila -macrophage interaction, we now demonstrate that  L. pneumophila  evades host cell apoptosis independent of SidF. In the absence of SidF,  L. pneumophila  was able to replicate, cause loss of mitochondria membrane potential, kill macrophages, and establish infections in lungs of mice. Consistent with this, deletion of BNIP3 and BCL-RAMBO did not affect intracellular  L. pneumophila  replication, macrophage death rates, and  in vivo  bacterial virulence. Abrogating mitochondrial cell death by genetic deletion of the effectors of intrinsic apoptosis, BAX, and BAK, or the regulator of mitochondrial permeability transition pore formation, cyclophilin-D, did not affect bacterial growth or the initial killing of macrophages. Loss of BAX and BAK only marginally limited the ability of  L. pneumophila  to efficiently kill all macrophages over extended periods.  L. pneumophila  induced killing of macrophages was delayed in the absence of capsase-11 mediated pyroptosis. Together, our data demonstrate that  L. pneumophila  evades host cell death responses independently of SidF during replication and can induce pyroptosis to kill macrophages in a timely manner.

Legionella pneumophila Strain 130b Evades Macrophage Cell Death Independent of the Effector SidF in the Absence of Flagellin