PapG II adhesin in the establishment and persistence of Escherichia coli infection in mouse kidneys.

Abstract

Most human pyelonephritogenic Escherichia coli express the PapG II adhesin. However, the role of the PapG II adhesin in enhancing the establishment and persistence of E. coli infection in the kidney is controversial. A pyelonephritogenic strain, EC114, which possesses one copy of the papG II gene, but without other virulence factors (such as S/F1C-fimbriae, hemolysin, and cytotoxic necrotizing factor 1) was selected for the construction of a papG II mutant. The resulting papG II mutant was confirmed by polymerase chain reaction, Southern hybridization, and agglutination assay, and designated as MEC114. We compared MEC114 with the parental strain (EC114) for colonization ability in the bladder and kidney of female BALB/c mice, which were challenged transurethrally with 50 microl of a low (5x10(4) CFU (colony-forming unit)) or high (5x10(8) CFU) dose of EC114 or MEC114 and assessed 1, 3, and 7 days after inoculation. Geometric means of quantitative bacterial counts in the kidney were significantly decreased when challenged with MEC114 on day 3 after inoculation, at both low and high dose (P<0.05), as compared with EC114. On the seventh day, both strains were mainly cleared from the kidney. Renal biopsy showed a similar degree of inflammatory response to both strains 1, 3, and 7 days after inoculation. In brief, the PapG II adhesin can enhance the early establishment of E. coli infection in the kidney, but the bacteria do not maintain infection owing to the host immune response.