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Renal scarring by mannose-sensitive adhesin of Escherichia coli type 1 pili
Y Mizunoe1, T Matsumoto, M Sakumoto
1Department of Bacteriology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Abstract:
Most Escherichia coli isolates from patients with pyelonephritis possess both pap (mannose-resistant) pili and type 1 (mannose-sensitive) pili. In the experimental pyelonephritis model of rats, the mannose-sensitive-piliated strain caused severe renal scarring, whereas the mannose-resistant or nonpiliated strain did not. Type 1 pili consist of several subunits; one major subunit and other minor subunits. One of the minor subunits, adhesin, is responsible for mannose-sensitive adhesion to eukaryotic cells. The role of adhesin was examined in scar formation after infection with a newly constructed adhesin-deficient mutant which has pilus structure but cannot agglutinate guinea pig erythrocytes. A mutant plasmid, pYMZ84, containing a deletion in the adhesin gene of type 1 pili, failed to agglutinate guinea pig erythrocytes even though the bacteria expressed pili morphologically indistinguishable from those produced by plasmid pSH2, carrying the intact genes for the type 1 pili. E. coli harboring pYMZ84 caused negligible or minimal renal scarring, whereas E. coli harboring pSH2 caused severe renal scarring in rats. These data suggest that the mannose-sensitive adhesin of type 1 pili stimulates renal scarring.
Insights
Mannose-sensitive adhesin on type 1 pili from Escherichia coli causes severe renal scarring in pyelonephritis models. This finding highlights adhesin
Area of Science:
- Microbiology
- Pathogenesis
- Urology
Background:
- Most Escherichia coli strains causing pyelonephritis have both pap (mannose-resistant) and type 1 (mannose-sensitive) pili.
- Type 1 pili are crucial for bacterial adhesion and pathogenesis.
- Adhesin, a minor subunit of type 1 pili, mediates mannose-sensitive adhesion to host cells.
Purpose of the Study:
- To investigate the role of adhesin in renal scar formation during experimental pyelonephritis.
- To determine if mannose-sensitive adhesion mediated by adhesin contributes to pyelonephritis pathogenesis.
Main Methods:
- Construction of an adhesin-deficient mutant of Escherichia coli using plasmid pYMZ84.
- Assessment of bacterial adhesion and hemagglutination properties of the mutant.
- Infection of a rat pyelonephritis model with wild-type and mutant strains.
- Evaluation of renal scarring severity post-infection.
Main Results:
- The adhesin-deficient mutant (pYMZ84) expressed morphologically normal pili but lacked hemagglutination activity.
- Escherichia coli harboring the intact type 1 pili genes (pSH2) caused severe renal scarring in rats.
- The adhesin-deficient mutant (pYMZ84) caused negligible or minimal renal scarring.
Conclusions:
- Mannose-sensitive adhesin of type 1 pili plays a critical role in stimulating renal scarring during pyelonephritis.
- Targeting type 1 pili adhesin may be a therapeutic strategy to prevent kidney damage in E. coli infections.