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The rfb locus from Pseudomonas aeruginosa strain PA103 promotes the expression of O antigen by both LPS‐rough and LPS‐smooth isolates from cystic fibrosis patients
Author(s) -
Evans David J.,
Pier Gerald B.,
Coyne Michael J.,
Goldberg Joanna B.
Publication year - 1994
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1994.tb00437.x
Subject(s) - pseudomonas aeruginosa , biology , antigen , microbiology and biotechnology , plasmid , locus (genetics) , lipopolysaccharide , recombinant dna , cystic fibrosis , strain (injury) , gene , bacteria , immunology , genetics , anatomy
Summary Strains of Pseudomonas aeruginosa initially isolated from patients with cystic fibrosis (CF) often express a smooth lipopolysaccharide (LPS) containing many long O side‐chain antigens, but once a chronic infection is established, strains recovered from these patients express little or no LPS O antigen. The genetic basis for this loss of O antigen expression by P. aeruginosa CF isolates is unknown. We report here that 20 CF isoiates of P. aeruginosa , 13 of which are LPS‐rough, were each capable of expressing serogroup 011 antigen when provided with the rfb iocus from P. aeruginosa serogroup 011 strain PA103 on the recombinant plasmid pLPS2. Eight of the thirteen LPS‐rough isolates co‐expressed another, presumably endogenous, O antigen when they contained pLPS2. Different subcloned regions of pLPS2 complemented distinct strains to restore endogenous O antigen expression. These data suggest that the loss of O antigen expression by P. aeruginosa CF isolates results from alterations specific to the rfb region, and is not due to mutations involving other loci or ancillary LPS genes.