作者: J.F. Poschet , J.C. Boucher , A.M. Firoved , V. Deretic
DOI: 10.1016/S0076-6879(01)36579-5
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摘要: Publisher Summary This chapter discusses the conversion to mucoidy in pseudomonas aeruginosa, as a potent human opportunistic pathogen causing chronic respiratory infections cystic fibrosis (CF). The persistent infection of CF lung is facilitated by biofilm mode growth mucoid, exopolysaccharide alginate-overproducing mutants P. aeruginosa selected during process colonization tract. molecular mechanism involves two pathways. more common pathway depends on activation alternative sigma factor Alg U via mutations gene termed mucA. In addition bacterial genetic factors, host environment contributes selection and formation bio films because encoding transmembrane conductance regulator (CFTR). alginate may play role resistance phagocytosis, scavenging reactive oxygen intermediates, number other biofilm-related phenomena. Alginate biofilms counteract processes elimination uptake killing macrophages neutrophils, potentially epithelial cells. describes methods, approaches, cell culture techniques, animal models used examine mucoid phenotype their pathogenesis CF.