In this study, bacterial attachment to rat tracheal surface was measured using three nonmucoid strains of Pseudomonas aeruginosa and bacterial growth after binding to tracheal surface was also tested. Brush injury on tracheal surface significantly increased bacterial attachment (1,190 to 1,600%); bacteria binding to brush-injured sites grew more rapidly than either nonbinding bacteria or those on intact trachea. A partial characterization of the binding sites for P. aeruginosa on either intact or injured tracheal surface also was performed. Treatment of injured tracheal surface with metaperiodate significantly inhibited attachment of P. aeruginosa, but trypsin treatment did not. In contrast, neither reagent had any effects on bacterial attachment to intact tracheal surface. These results suggest that brush injury on tracheal surface produces new binding sites as a receptor for P. aeruginosa, and that this receptor has carbohydrates as important components and that it is not a protein receptor. In addition, in order to determine what the dominant sugar of this receptor was, we tested the inhibition of bacterial attachment with monosaccharide, neuraminidase, and lectin. Treatment of bacteria with N-acetylneuraminic acid (NANA) dramatically inhibited bacterial attachment to injured trachea. However, NANA also inhibited the growth of this organism. Moreover, neither neuraminidase nor lectin data suggested that the dominant sugar of the receptor was NANA. Our data go so far as to confirm that the major component of the receptor of nonmucoid strains of P. aeruginosa on brush-injured trachea is carbohydrates; it is still unclear what kind of sugar is the dominant component of the receptor.(ABSTRACT TRUNCATED AT 250 WORDS)