Swimming Motility Mediates the Formation of Neutrophil Extracellular Traps Induced by Flagellated Pseudomonas aeruginosa.

摘要: Pseudomonas aeruginosa is an opportunistic pathogen causing severe infections often characterized by robust neutrophilic infiltration. Neutrophils provide the first line of defense against P. aeruginosa. Aside from their conferred phagocytic activity, neutrophils also release neutrophil extracellular traps (NETs) to immobilize bacteria. Although NET formation important antimicrobial process, details its mechanism are largely unknown. The identity main components responsible for triggering unclear. In this study, our focus was identify bacterial factors mediating and gain insight into underlying mechanism. We found that in exponential growth phase promoted strong human while NET-inducing ability dramatically decreased at later stages growth. identified flagellum as primary component inducing extrusion flagellum-deficient bacteria remained seriously impaired formation. Purified flagellin, monomeric flagellum, does not stimulate neutrophils. aeruginosa-induced independent flagellum-sensing receptors TLR5 NLRC4 both mouse Interestingly, we flagellar motility, binding per se, mediates induced flagellated Immotile, motor-deficient strains producing paralyzed flagella did induce Forced contact between immotile restored ability. Both motAB motCD genetic loci encoding motor genes contribute maximal release; however play a more role. Phagocytosis superoxide production were dependent upon functional flagellum. Taken together, herein presented time organelle planktonic release. Furthermore, rather than on host cells, required