CHLAMYDIA-TRACHOMATIS GLYCOSAMINOGLYCAN-DEPENDENT AND INDEPENDENT ATTACHMENT TO EUKARYOTIC CELLS

Chlamydia trachomatis consists of two biovars, lymphogranuloma venereu m (LGV) and trachoma, that differ in their infectivity in vivo and in vitro. Although addition of exogenous heparin or heparan sulfate in vi tro effectively inhibits infectivity of both biovars and inhibits LGV biovar attachment to host cells, trachoma biovar attachment was only m odestly inhibited (similar to 30%) by exogenous heparin. To dissect th e relationship of heparin inhibition of attachment and infectivity, a heparan sulfate lyase (heparitinase) was used to treat organisms and e valuated for changes in attachment and infectivity. In contrast to hep aritinase-treated LGV biovar organisms that lose their ability to atta ch and infect, treatment of trachoma biovar organisms with a concentra tion of heparitinase sufficient to reduce trachoma biovar infectivity by >90%, only inhibited attachment to host cells by similar to 40%. Si gnificantly, attachment could be fully restored for heparitinase-treat ed organisms of both biovars with exogenous heparan sulfate; however, the coating of the trachoma biovar organisms with heparan sulfate rend ered the trachoma biovar similar to the phenotype of the LGV biovar by >90% sensitivity to heparin inhibition of attachment. These data sugg est that the LGV biovar used predominantly a heparin-inhibitable mecha nism for attaching to host cells, whereas the trachoma biovar used a h eparin-independent means in addition to a heparin-dependent mechanism to adhere to host cells. Once attached, the trachoma biovar, neverthel ess, relied on the heparin-dependent pathway to enter host cells. (C) 1997 Academic Press Limited