Abstract
Chlamydia is an obligate intracellular pathogen that develops in the host cell in a vacuole termed the chlamydial inclusion. The prevailing concept of the chlamydial inclusion is of a parasitophorous vacuole. Here, the inclusion is the recipient of one-way host-pathogen interactions thus draining nutrients from the cell and negatively impacting it. While Chlamydia orchestrates some aspects of cell function, recent data indicate host cells remain healthy up until, and even after, chlamydial egress. Thus, while Chlamydia relies on the host cell for necessary metabolites, the overall function of the host cell, during chlamydial growth and development, is not grossly disturbed. This is consistent with the obligate intracellular organism's interest to maintain viability of its host. To this end, Chlamydia expresses inclusion membrane proteins, Incs, which serve as molecular markers for the inclusion membrane. Incs also contribute to the physical structure of the inclusion membrane and facilitate host-pathogen interactions across it. Given the function of Incs and the dynamic interactions that occur at the inclusion membrane, we propose that the inclusion behaves similarly to an organelle-albeit one that benefits the pathogen. We present the hypothesis that the chlamydial inclusion acts as a pathogen-specified parasitic organelle. This representation integrates the inclusion within existing subcellular trafficking pathways to divert a subset of host-derived metabolites thus maintaining host cell homeostasis. We review the known interactions of the chlamydial inclusion with the host cell and discuss the role of Inc proteins in the context of this model and how this perspective can impact the study of these proteins. Lessons learnt from the chlamydial pathogen-specified parasitic organelle can be applied to other intracellular pathogens. This will increase our understanding of how intracellular pathogens engage the host cell to establish their unique developmental niches.
Highlights
Bacteria that seek refuge from host defenses within a cell encounter a hostile intracellular environment
Given the function of Incs and the dynamic interactions that occur at the inclusion membrane, we propose that the inclusion behaves to an organelle-albeit one that benefits the pathogen
While Rab proteins are specific for different subcellular compartments, a given Rab protein functions at every location within the cell—even, it would seem, at pathogen-specified parasitic organelles
Summary
Bacteria that seek refuge from host defenses within a cell encounter a hostile intracellular environment. Given these characteristics of an organelle, we hypothesize that the chlamydial inclusion is a pathogen-specified parasitic organelle (Figure 1) In this context, the “chlamydial” organelle (i) serves the specific function of promoting chlamydial growth and development, (ii) is membrane-bound and identified through specific surface, cytoplasmically exposed markers: the Incs, and (iii) intercepts proteins/vesicles with specific trafficking signals (e.g., YGRL) (Moore et al, 2011; Kabeiseman et al, 2014). These data indicate that the ultimate composition and identity of the chlamydial inclusion rely on its ability to interact with multiple subcellular pathways This is consistent with “fitting in” within a network of organelles that engage in cross-talk to effectively orchestrate host cell functionality. The view of the inclusion as a pathogen-specified parasitic organelle integrates the developmental expression of Incs with temporal characteristics of the inclusion and the bacteria themselves in ways that allow the inclusion to have a minimal impact on the health of the host cell
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
