The abstract is read at the publisher; the summary is JClub's.
Swimming motility and type IV pili in Pseudomonas aeruginosa shape physical contact with macrophages, reducing phagocytic uptake when motility or T4P function is disrupted.
- Why it matters: Chronic lung infection involves diverse P. aeruginosa populations, but how bacterial heterogeneity alters macrophage processing is not well defined.
- What they did: Using an attenuated T3SS-deficient mutant to isolate phagocytosis susceptibility, the authors applied Tn-seq to find fitness factors under phagocytic selection, then used live-cell imaging to test attachment and surface accumulation.
- The result: Motility gene disruptions lowered macrophage uptake by destabilizing bacterial attachment and surface accumulation; clinical isolates with reduced swimming or twitching showed similar uptake defects, and restoring T3SS revealed an attenuated killing phenotype for the non-flagellated, hyper-piliated ΔfliC ΔpilT mutant.
The findingWhy it mattersWhat they didThe result
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