Safe haven under constant attack-TheChlamydia-containing vacuole

Abstract

Chlamydia belong to the group of obligate intracellular bacteria that reside in a membrane bound vacuole during the entire intracellular phase of their life cycle. This vacuole called inclusion shields the bacteria from adverse influences in the cytosol of the host cell like the destructive machinery of the cell-autonomous defence system. The inclusion thereby prevents the digestion and eradication in specialised compartments of the intact and viable cell called phagolysosomes or autophagolysosomes. It is becoming more and more evident that keeping the inclusion intact also prevents the onset of cell intrinsic cell death programmes that are activated upon damage of the inclusion and direct the cell to destruct itself and the pathogen inside. Chlamydia secrete numerous proteins into the inclusion membrane to protect and stabilise their unique niche inside the host cell. We will focus in this review on the diverse attack strategies of the host aiming at the destruction of the Chlamydia-containing inclusion and will summarise the current knowledge on the protection mechanisms elaborated by the bacteria to maintain the integrity of their replication niche.

The chlamydial deubiquitinase Cdu1 supports recruitment of Golgi vesicles to the inclusion

“…Although Chlamydia does not reside in the cytosol of host cells for extended times, a leaky or perforated inclusion membrane during late stage infections or as a consequence of cell autonomous immune attack may offer targets for activating autophagy (Fischer & Rudel, ; Weber et al, ). In Ctr Tn‐ cdu1 , but not in wild‐type infected cells we find the inclusion decorated with ubiquitin and recruitment of autophagy proteins already during the replicative phase of the bacteria (24 hpi) when the inclusion is still intact (data not shown).…”

Maraviroc, celastrol and azelastine alter Chlamydia trachomatis development in HeLa cells

“…Additionally, since chlamydial Inc proteins are important in the assembly of an inclusion-stabilizing scaffold of intermediate filaments [71], it is interesting to speculate that these proteins may be a direct target of Az. Generally speaking, changes in chlamydial membrane integrity would have important consequences for chlamydial and host cell survival [2], which might explain the observed anti-chlamydial effects of Az in our study. Even though chlamydial infectivity upon discontinuation of Az exposure in 48 h of further HeLa/ CtE culture did not differ significantly from infectivity upon continued exposure, the 1000-fold increase in chlamydial infectivity might still be biologically relevant ().…”

“… Chlamydia are Gram-negative obligate intracellular bacteria with a unique bi-phasic life cycle, comprising infectious extracellular forms called elementary bodies (EBs) and non-infectious intracellular, metabolically active, replicating forms called reticulate bodies (RBs) [1, 2]. These bacteria are important pathogens causing acute or chronic clinical diseases as well as asymptomatic infections in human or animal host species [3].…”

Transmembrane substrates of type three secretion system injectisomes

“…Many are localized in the membrane that contains the injectisome translocon: e.g. Tir is found in the plasma membrane, SseF and SseG in the SCV membrane and Incs in the Chlamydia inclusion membrane [76–78]. In contrast, following its delivery through the SCV membrane, the Salmonella TME SteD is found in the trans -Golgi network (TGN) and in endosomes including major histocompatibility complex (MHC)II compartments [73].…”