RENAL SCARRING BY MANNOSE-SENSITIVE ADHESIN OF ESCHERICHIA-COLI TYPE-1 PILI

Most Escherichia coli isolates from patients with pyelonephritis posse ss both pap (mannose-resistant) pili and type 1 (mannose-sensitive) pi li. In the experimental pyelonephritis model of rats, the mannose-sens itive-piliated strain caused severe renal scarring, whereas the mannos e-resistant or nonpiliated strain did not. Type 1 pili consist of seve ral subunits; one major subunit and other minor subunits. One of the m inor subunits, adhesin, is responsible for mannose-sensitive adhesion to eukaryotic cells. The role of adhesin was examined in scar formatio n after infection with a newly constructed adhesin-deficient mutant wh ich 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 tho ugh the bacteria expressed pili morphologically indistinguishable from those produced by plasmid pSH2, carrying the intact genes for the typ e 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.