Abstract
Background. Previous works suggest that sugars can have a beneficial effect on C. trachomatis (CT) survival and virulence. In this study, we investigated the effect of different sugars on CT infectivity, elucidating some of the molecular mechanisms behind CT-sugar interaction. Methods. CT infectivity was investigated on HeLa cells after 2 hour-incubation of elementary bodies (EBs) with glucose, sucrose, or mannitol solutions (0.5, 2.5, 5.0 mM). The effect of sugars on EB membrane fluidity was investigated by fluorescence anisotropy measurement, whereas the changes in lipopolysaccharide (LPS) exposure were examined by cytofluorimetric analysis. By means of a Western blot, we explored the phosphorylation state of Focal Adhesion Kinase (FAK) in HeLa cells infected with EBs pre-incubated with sugars. Results. All sugar solutions significantly increased CT infectivity on epithelial cells, acting directly on the EB structure. Sugars induced a significant increase of EB membrane fluidity, leading to changes in LPS membrane exposure. Especially after incubation with sucrose and mannitol, EBs led to a higher FAK phosphorylation, enhancing the activation of anti-apoptotic and proliferative signals in the host cells. Conclusions. Sugars can increase CT infectivity and virulence, by modulating the expression/exposure of chlamydial membrane ligands. Further in-depth studies are needed to better understand the molecular mechanisms involved.
Highlights
Chlamydia trachomatis (CT) is the causative agent of the most common bacterial sexually transmitted infection (STI) worldwide [1].C. trachomatis (CT) serovars from D to K are responsible for common uro-genital infections, potentially evolving into serious complications, as pelvic inflammatory disease (PID), and tubal infertility [2].CT is an obligate intracellular pathogen, characterized by a biphasic development cycle [3].The extracellular, infectious elementary bodies (EBs) enter epithelial mucosal cells and differentiate into reticulate bodies (RBs) in a membrane bound compartment
We ruled out any effect of significantly increase EB membrane fluidity, with no effect on sugars on the epithelial cells
We can speculate that the effect of sugars is not limited to one specific serovar: in a previous work [10], we found that women with CT uro-genital infections are characterized by higher levels of urinary sucrose, and mannitol, irrespective of the chlamydial serovars
Summary
The extracellular, infectious elementary bodies (EBs) enter epithelial mucosal cells and differentiate into reticulate bodies (RBs) in a membrane bound compartment (i.e. chlamydial inclusion). After several rounds of replication (48–72 h post-infection), intracellular RBs start to re-differentiate into EBs; at the end of the cycle, EBs are released from the host cell, ready to infect neighboring cells [4]. Several works have focused on the role of sugars during the CT development cycle and its pathogenic process [5,6,7,8]. CT infectivity was investigated on HeLa cells after 2 hour-incubation of elementary bodies (EBs) with glucose, sucrose, or mannitol solutions (0.5, 2.5, 5.0 mM). The effect of sugars on EB membrane fluidity was investigated by fluorescence anisotropy measurement, whereas the changes in lipopolysaccharide (LPS) exposure were examined by cytofluorimetric analysis. By means of a Western blot, we explored the phosphorylation state of Focal Adhesion Kinase (FAK) in HeLa cells infected with
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