Heparan sulfate-like glycosaminoglycan is a cellular receptor for Chlamydia pneumoniae

Chlamydia pneumoniae is an important human intracellular pathogen; however, the pathogenesis of C. pneumoniae infection is poorly understood, and the bacterial adherence mechanism to host cells is unknown. This study examined the role of glycosaminoglycans (GAGs) in the adhesion of C. pneumoniae to eukaryotic cells. Heparin and heparan sulfate were found to inhibit the att achment of C. pneumoniae to human epithelial cells. Reduction in infectivit y resulted from the binding of heparin to the organism. Enzymatic removal o f heparan sulfate moieties from the host cell surface led to a marked decre ase in C. pneumoniae infectivity. Mutant CHO cell lines that were defective in heparan sulfate biosynthesis were less susceptible to C. pneumoniae inf ection than was the wild-type cell line. However, preincubation of the GAG- deficient CHO cells with exogenous heparin greatly increased infectivity.