Abstract
The role of glycosaminoglycans (GAGs) in the invasion of host cells by Chlamydia pneumoniae strains TW-183 and A-03 was investigated and compared with the role of invasion by C. trachomatis serovars L2 and E. The quantities of epithelial and endothelial cell-surface GAGs, as well as chlamydial elementary body (EB)-surface GAGs, were investigated. When specific enzymes were used to cleave GAGs from host cells or EBs, decreased infection rates were observed with C. pneumoniae and C. trachomatis serovar L2 in epithelial cells, but not in endothelial cells. Larger decreases in infection occurred with enzyme-treated EBs in GAG-deficient Chinese hamster ovary (CHO) cells. EBs grown in GAG-deficient CHO cells resulted in lower amounts of EB surface GAGs and decreased infectivity of epithelial cells. The results indicate that C. pneumoniae and C. trachomatis L2 EB-surface GAGs and host cell-surface GAGs are involved in invasion of bronchial epithelial cells but not of human umbilical vein endothelial cells.
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