Chlamydia trachomatis Co-opts the FGF2 Signaling Pathway to Enhance Infection

• DOI: 10.1371/journal.ppat.1002285
• Publication Date: 2011-10-06T21:56:39Z
• Authors: Jung Hwa Kim; Shaobo Jiang; Cherilyn A. Elwell; Joanne N. Engel
• Keywords: Infectivity

The molecular details of Chlamydia trachomatis binding, entry, and spread are incompletely understood, but heparan sulfate proteoglycans (HSPGs) play a role in the initial binding steps. As cell surface HSPGs facilitate interactions many growth factors with their receptors, we investigated HSPG-dependent C. infection. Here, report novel finding that Fibroblast Growth Factor 2 (FGF2) is necessary sufficient to enhance host cells an manner. FGF2 binds directly elementary bodies (EBs) where it may function as bridging molecule EBs FGF receptor (FGFR) on surface. Upon EB FGFR activated locally contributes bacterial uptake into non-phagocytic cells. We further show infection stimulates fgf2 transcription enhances production release through pathway requires protein synthesis activation Erk1/2 signaling independent activation. Intracellular replication bacteria results proteosome-mediated degradation high weight (HMW) isoforms increased amounts low (LMW) isoforms, which released upon death. Finally, demonstrate vivo relevance these findings by showing conditioned medium from infected enriched for LMW FGF2, accounting its ability infectivity additional rounds Together, utilizes multiple mechanisms co-opt spread.