Bacteria-associated fibronectin does not enhance Chlamydia trachomatis infectivity in vitro

The molecules responsible for mediating attachment of pathogenic bacteria to their host cells are essential determinants of the pathogen's success. Staphylococci, streptococci, and gonococci are known to utilize fibronectin to mediate adhesion and/or entry into eukaryotic cells. It has been shown that Chlamydia trachomatis binds fibronectin via a heparan sulfate-lyase sensitive molecule on the surface of the bacteria. Because heparan sulfate-lyase treated Chlamydia are markedly reduced in infectivity, we hypothesized that fibronectin might be acting as an intermediate to form a molecular bridge between heparan sulfate-like molecules on the surface of Chlamydia and integrins on the host cell. To test this question, fibronectin-deficient C. trachomatis were used in a series of infectivity assays whereby exogenous fibronectin was added to the inoculum. At concentrations up to 100 ug/ml fibronectin did not modulate C. trachomatis infectivity. However, at high fibronectin concentrations (1 mg/ml) bacterial infectivity was reduced. These data suggest that, unlike several other microbial pathogens, C. trachomatis does not utilize fibronectin to mediate infectivity in vitro.