Abstract
Prokaryotic communities coordinate quorum behaviour in response to external stimuli to control fundamental processes including inter-bacterial communication. The obligate intracellular bacterial pathogen Chlamydia adopts two developmental forms, invasive elementary bodies (EBs) and replicative reticulate bodies (RBs), which reside within a specialised membrane-bound compartment within the host cell termed an inclusion. The mechanisms by which this bacterial community orchestrates different stages of development from within the inclusion in coordination with the host remain elusive. Both prokaryotic and eukaryotic kingdoms exploit ion-based electrical signalling for fast intercellular communication. Here we demonstrate that RBs specifically accumulate potassium (K+) ions, generating a gradient. Disruption of this gradient using ionophores or an ion-channel inhibitor stalls the Chlamydia lifecycle, inducing persistence. Using photobleaching approaches, we establish that the RB is the master regulator of this [K+] differential and observe a fast K+ exchange between RBs revealing a role for this ion in inter-bacterial communication. Finally, we demonstrate spatio-temporal regulation of bacterial membrane potential during RB to EB differentiation within the inclusion. Together, our data reveal that Chlamydia harnesses K+ to orchestrate host sensing, inter-bacteria communication and pathogen differentiation.
Highlights
Chlamydia trachomatis are obligate intracellular bacteria responsible for the most prevalent bacterial sexually transmitted infection worldwide [1]
We show that reticulate bodies (RBs) lose K+ during their differentiation into elementary bodies (EBs), which equilibrates with the inclusion lumen
[K+]whole. inclusion ever, the probe and microscopy applied only allowed the measurement of whole inclusion (EB, RB and inclusion lumen (IL)) as well as its immediate environment by epifluroescence microscopy
Summary
Chlamydia trachomatis are obligate intracellular bacteria responsible for the most prevalent bacterial sexually transmitted infection worldwide [1]. RBs differentiate into EBs, which are released into the extracellular environment In addition to these two forms, transient persistent bodies (PBs) form in cell culture models, which can revert to RB and complete the infection cycle when favourable conditions are restored. It is known that Chlamydiae use a variety of effectors to manipulate or hijack host processes [12] This communication is unilateral and does not satisfy the requirement for the bacteria to sense conditions in the host. We show that persistence induced by a range of stimuli induces an abnormality in the [K+ ] ratio between the bacteria and the cytosol or the inclusion lumen demonstrating the importance of the [K+ ] differential in the Chlamydia lifecycle, suggestive of a bacterial host-stress sensing mechanism. K+ electrical signalling to sense the host cell, ensure community communication and to orchestrate critical steps in the Chlamydia lifecycle
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