An extraintestinal, pathogenic isolate of Escherichia coli (O4/K54/H5) can produce a group 1 capsule which is divergently regulated from its constitutively produced group 2, K54 capsular polysaccharide.

摘要: We are studying an O4/K54/H5 Escherichia coli bacteremic isolate (CP9) as a model pathogen for extraintestinal infection. Its group 2, K54 capsular polysaccharide is important virulence determinant and confers serum resistance. In this study the effect of 1 capsule regulators, RcsA, RcsB, Lon protease, on regulation CP9's polysaccharides was assessed. It established that in presence multicopy rcsA or with disruption lon, CP9 can be induced to produce capsule. present background regulate expression fashion similar described K-12 strains. Two independent 2 gene protein fusions (cl1.29::TnphoA cl1.137::TnphoA) were used evaluate effects these regulators production. Disruption lon resulted 1.9-fold (TR293 [cl1.29::TnphoA lon-146]) 3.4-fold (TR1373 [cl1.137::TnphoA decreases fusion activity at 28 degrees C, relative baseline level. However, 42 C only 1.2- 1.4-fold, respectively. Inactivation both rcsB restored levels but partial restoration seen higher temperatures. To assess whether differences reflected functional change production, 80% normal human (NHS) tested against TR93 (lon-146). Since protects bactericidal NHS, decrease its production results increase sensitivity. Viable counts increased 10-fold NHS over 3 h expected. contrast CP9, (lon-146) incurred loss viability under same conditions. The RcsA (lon 146) consequence disruption; therefore, conjunction cl1::TnphoA data establish negative regulator polysaccharide. Furthermore, also suggest existence another Lon-sensitive which active