Renal scars are thought to be the end stage of chronic pyelonephritis. In the experimental pyelonephritis model of rats, mannose sensitive (MR) -piliated strain caused severe renal scarring whereas mannose resistant (MS) - or non-piliated strain did not and this renal scarring was suppressed by treatment with superoxide dismutase. The piliation of bacteria was compared for their capacity to interact with human polymorphonuclear leukocytes (PMNs). MS-piliated strain stimulated superoxide production of PMNs two times more than MR- and non-piliated strains did. MS 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. To investigate the role of adhesin in renal scarring, we constructed the adhesin-deficient mutant which has pilus structure but cannot agglutinate guinea pig erythrocytes. A recombinant plasmid pSH2 carries the genomic information for the synthesis and expression of functional MS pili of E.coli. A mutant, pYMZ84, containing a deletion in the adhesin gene of MS pili failed to agglutinate guinea pig erythrocytes even though the bacteria expressed pili morphologically and antigenically indistinguishable from those produced by plasmid pSH2, carrying the intact genes for the MS pili. E.coli harboring pYMZ84 did not cause renal scarring whereas E.coli harboring pSH2 caused severe renal scarring in rats. PMN showed significantly high peak response of chemiluminescence and most of oxidative burst occurred within five minutes after stimulating with MS-piliated bacteria compared with non- or adhesin mutant-piliated bacteria. These data suggest that MS pili confer the bacteria to cause large amount of oxidative burst of PMNs within a few minutes and lead to the tissue damage in the infected organ and adhesin of MS pili play a central role in this process.