Host-pathogen reorganisation during host cell entry by Chlamydia trachomatis

Abstract

Chlamydia trachomatis is obligate intracellular bacterial pathogen that remains a significant public health burden worldwide. A critical early event during infection is chlamydial entry into non-phagocytic host epithelial cells. Like other Gram-negative bacteria, C. trachomatis uses a type III secretion system (T3SS) to deliver virulence effector proteins into host cells. These effectors trigger bacterial uptake and promote bacterial survival and replication within the host cell. In this review, we highlight recent cryo-electron tomography that has provided striking insights into the initial interactions between Chlamydia and its host. We describe the polarised structure of extracellular C. trachomatis elementary bodies (EBs), and the supramolecular organisation of T3SS complexes on the EB surface, in addition to the changes in host and pathogen architecture that accompany bacterial internalisation and EB encapsulation into early intracellular vacuoles. Finally, we consider the implications for further understanding the mechanism of C. trachomatis entry and how this might relate to those of other bacteria and viruses.

The cellular ceramide transport protein CERT promotesChlamydia psittaciinfection and controls bacterial sphingolipid uptake

“…(Fechtner, Galle, & Hegemann, ; Norkin, Wolfrom, & Stuart, ). Uptake requires the delivery of bacterial proteins into the host cell cytosol using a type III secretion system (Hsia, Pannekoek, Ingerowski, & Bavoil, ; Hybiske & Stephens, ; Nans, Ford, & Hayward, ). One of these effectors is Tarp that remodels the actin cytoskeleton and induces specific antiapoptotic signalling pathways (Clifton et al, ; Mehlitz et al, ).…”

Chlamydia trachomatis: the Persistent Pathogen

“…This is followed by chlamydia-induced actin remodeling that facilitates entry of the microorganism into the cytoplasm (4). The EBs become internalized into endocytic vacuoles, which then combine to form an intracytoplasmic inclusion (5). Within this structure, the EBs transform into the noninfectious replicative form of the organism called the reticulate body (RB).…”

Peptidoglycan in obligate intracellular bacteria

“…Chlamydiae are tropic for endothelial, epithelial and monocyte/macrophage cells and even primitive macrophage-like cells such as amoebae (Kebbi-Beghdadi and Greub, 2014). They secrete effector proteins through a type 3 secretion system to trigger dramatic rearrangement of the host cytoskeleton resulting in engulfment of the bacterium (Nans et al, 2015). Once phagocytosed by the host cell, Chlamydiae remodel the phagocytic vacuole, resulting in a specialised membrane-surrounded organelle, called inclusion, that provides a protected environment for replication (Nans et al, 2015).…”

“…They secrete effector proteins through a type 3 secretion system to trigger dramatic rearrangement of the host cytoskeleton resulting in engulfment of the bacterium (Nans et al, 2015). Once phagocytosed by the host cell, Chlamydiae remodel the phagocytic vacuole, resulting in a specialised membrane-surrounded organelle, called inclusion, that provides a protected environment for replication (Nans et al, 2015). The chlamydial cell type that is engulfed is the dispersal form known as the elementary body, a non-replicative and poorly metabolically active cell type.…”

“…The chlamydial cell type that is engulfed is the dispersal form known as the elementary body, a non-replicative and poorly metabolically active cell type. Upon uptake, the elementary body differentiates within the inclusion into the replicative reticulate body which is no longer infectious (Nans et al, 2015). Chlamydiales are amongst the few known bacteria that lack FtsZ, the bacterial tubulin homolog that organizes the divisome complex at midcell to direct septal peptidoglycan synthesis and facilitates cytokinesis (Busiek and Margolin, 2015).…”