Binding of Elementary Bodies by the Opportunistic Fungal Pathogen or Soluble β-Glucan, Laminarin, Inhibits Infectivity.

Microbial interactions represent an understudied facet of human health and disease. In this study, the interactions that occur between and the opportunistic fungal pathogen, were investigated. is a common component of the oral and vaginal microbiota responsible for thrush and vaginal yeast infections. Normally, exist in the body as yeast. However, disruptions to the microbiota create conditions that allow expanded growth of , conversion to the hyphal form, and tissue invasion. Previous studies have shown that a myriad of outcomes can occur when interacts with pathogenic bacteria. To determine if physically interacts with , we incubated chlamydial elementary bodies (EB) in medium alone or with yeast or hyphal forms for 1 h. Following incubation, the samples were formaldehyde-fixed and processed for immunofluorescence assays using anti-chlamydial MOMP or anti- chlamydial LPS antibodies. Replicate samples were replenished with culture medium and incubated at 35°C for 0-120 h prior to fixation for immunofluorescence analysis or collection for EB infectivity assays. Data from this study indicates that both serovar E and EB bind to yeast and hyphal forms. This interaction was not blocked by pre-incubation of EB with the cell wall components, mannan or β-glucans, suggesting that EB interact with a cell wall protein or other structure. Bound EB remained attached to for a minimum of 5 days (120 h). Infectivity assays demonstrated that EB bound to are infectious immediately following binding (0h). However, once bound to , EB infectivity decreased at a faster rate than EB in medium alone. At 6h post binding, 40% of EB incubated in medium alone remained infectious compared to only 16% of EB bound to . Likewise, pre-incubation of EB with laminarin, a soluble preparation of β-glucan, alone or in combination with other fungal cell wall components significantly decreases chlamydial infectivity in HeLa cells. These data indicate that interactions between EB and inhibit chlamydial infectivity, possibly by physically blocking EB interactions with host cell receptors.