in our current study , we found that early exponential growth phase cultures of p. aeruginosa elicited the most robust net release and presence of a functional flagellum was essential for this process .
forced contact of immotile p. aeruginosa with pmns restored their ability to trigger maximal net extrusion . 

p. aeruginosa flagellin alone was unable to induce net release . in a genetic complementation study we found that both , motab and motcd loci of p. aeruginosa
thus , we identified flagellar swimming motility as a novel microbial factor crucial to pmn activation and net formation .
although it is undocumented whether nets are present at early stages of cf lung disease , bacterial motility - fueled net formation likely occurs at this initial phase because early cf clinical isolates of p. aeruginosa typically express flagellum and pmns are also present ( fig .  1 ) .
the interaction of pmns with early forms of p. aeruginosa must be critical to determine later progression of cf lung disease .
important questions to be answered are why nets released at this early stage would be incapable of clearing p.
aeruginosa infection and instead drive bacterial adaption toward an aflagellated , biofilm - forming phenotype . over the course of cf lung disease , p. aeruginosa down - regulates its flagellum expression . in chronic cf airways ,
p. aeruginosa mainly exist in 3-dimensional ,  suspension biofilms  also called non - attached aggregates ( fig .  1 ) .
these suspension biofilms surrounded by pmns represent the characteristic clinical picture in chronic cf airways .
biofilms are dynamic structures , and motile , flagellated bacteria likely break free from biofilms in chronic cf , possibly interacting with pmns ( fig .  1 ) .
this is supported by recent data showing that p. aeruginosa flagellin is detected in sputa of chronic cf patients .
a minor population of flagellated p. aeruginosa in chronic cf airways could also have been marginalized so far because this topic has not been intensely investigated yet , and this population is hard to study and could have been overlooked in the presence of much more abundant biofilm - bound bacteria accumulating well - characterized mutations ( muca , lasr ) .
conclusions with respect to the population structure of p. aeruginosa in cf have largely been generalized based on results obtained on single bacterial isolates , although high levels of phenotypic diversity among p. aeruginosa isolates within individual cf patients have already been noted . a small population of flagellated p. aeruginosa could be found in cf airways while most p. aeruginosa are present in form of alginate - producing , elastase - negative bacteria .
muca mutations drive the mucoid , biofilm - forming phenotype , lasr mutations contribute to pmn recruitment while outbreaks of flagellated bacteria from biofilms could be mainly responsible for pmn activation and net release .
pmns quickly and easily recognize motile , flagellated forms of p. aeruginosa and launch their robust effector mechanisms including net release in response to them . on the other hand , bacterial biofilms
therefore , the way motile p. aeruginosa interacts with pmns , the cell type representing most of cells found in chronic cf airways , is likely an important factor in influencing the progression of cf lung disease despite the fact that planktonic forms of p. aeruginosa are outnumbered by those found in biofilms ( fig .  1 ) .
overall , we speculate that p. aeruginosa motility - driven pmn activation has clinical relevance not only at initial but also later stages of cf airway disease .
 abstractneutrophil extracellular trap ( net ) formation represents a unique effector function of neutrophils ( pmn ) . 
 the mechanism of net release in response to bacteria is largely unknown . 
 we studied the process by which pseudomonas aeruginosa , an opportunistic pathogen , interacts with primary pmns , and found that flagellar swimming motility of the bacterium is essential for inducing net extrusion . 
 cystic fibrosis ( cf ) lung disease is associated with p. aeruginosa infection and pmn - dominated inflammation . 
 although nets are abundant in cf airways , the main factors triggering net release in cf remain unclear . 
 our study implicates that motile p. aeruginosa is a strong net - inducer in cf . in early stages of cf lung disease flagellated , 
 motile isolates of p. aeruginosa are characteristic and their interactions with pmns could lead to net formation . in chronic cf 
 , p. aeruginosa down - regulates its flagellum expression to avoid recognition by the immune system and forms biofilms . flagellated bacteria , however , are released from biofilms and could interact with pmns to form nets . 
 although flagellated forms likely represent only a small fraction of the total p. aeruginosa load in chronic cf , net release induced by them could have a significant impact on inflammation and lung function since flagellated forms trigger the most robust response of the immune system including pmns.overall , we speculate that net formation driven by motile p. aeruginosa could be a novel , significant contributor to pathogenesis at both , early and late stages of cf lung disease . 
Flagellar motility drives 
Flagellated 
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