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Biofilm Dispersal and Exacerbations of Cystic Fibrosis Lung Disease

机译:囊性纤维化肺病的生物膜弥散和加重

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We read with interest the recent comments by VanDevanter et al. on the relative contributions of biofilm-dwelling and planktonic, that is, free living forms of Pseudomonas aeruginosa to acute exacerbations of cystic fibrosis (CF) lung disease. The concept put forward of "bacterial blooms" involving generation of more motile daughter cells from established biofilms is biologically plausible. Indeed, this process has recently been described in flow-thru models of P. aeruginosa biofilms using clinical isolates from adult CF patients and the term "seeding dispersal" applied. There are suggestions that seeding dispersal is controlled by the quorum sensing system and may be triggered by a variety of factors including depletion of crucial nutrients or potential build up of toxins within the depths ("core") of mature biofilms. There is also the possibly that dispersal occurs as a consequence of phage-mediated cell lysis.
机译:我们感兴趣地阅读了VanDevanter等人的最新评论。生物膜驻留和浮游生物(即铜绿假单胞菌的自由生活形式)对囊性纤维化(CF)肺病急性加重的相对贡献。提出的“细菌繁殖”概念涉及从已建立的生物膜中产生更多的运动子细胞,这在生物学上是合理的。实际上,最近已经使用来自成人CF患者的临床分离株在铜绿假单胞菌生物膜的流通模型中描述了该过程,并且使用了术语“播种散播”。有建议认为,种子散播是由群体感应系统控制的,并且可能由多种因素触发,包括重要营养物质的消耗或成熟生物膜深度(“核心”)内潜在的毒素堆积。还可能由于噬菌体介导的细胞裂解而发生分散。

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