Recently become quite interested in the lifecyle and molecular bio of chlamydia. Is it right that the chlamydia gets into host cell through endocytosis and live within phagosome? Have read paper that Chlamydia can block the host cell's apoptosis and NO synthesis through multiple pathway. If the chlamydia stays in the phagosome how can it control such behaviours of the hosts? Do the chlamydia control the host cell by secreting some chemical factors? what are the key factors secreted by chlamydia? how can these factors pass the phagosome membrane, get released in the host and influence the pathways of the host? Thanks! Also could reference be included?
In addition what are other key points in the life of chlamydia, and could some key articles be recommended of chlamydia? Thanks very much!
Chlamydia has an extraordinary lifestyle. It is taken up by the host cell through endocytosis, but the endosome is unique in that is does not fuse with lysosome, i.e. no phagolysosome, thereby evading degradation. The endosome lives like an additional cell organelle for which it is known as inclusion. Lodging near the Golgi, it chokes other cell organelles for vital compounds, as a parasite.
It then controls other cell organelles including the nucleus by secreting a cohort of virulence effectors. The most interesting of these effectors is inclusion membrane proteins, or Incs. Incs are injected into the cytosol or organelles through a molecular syringe of type III secretory system (T3SS) present on the membrane of the inclusion.
These are very good readings:
Article Reconceptualizing the chlamydial inclusion as a pathogen-spe...
Article Chlamydia cell biology and pathogenesis
Hello Zonghan,
The first and most important immune response to Chlamydia infection is a local one, whereby immune cells such as leukocytes are recruited to the site of infections, and subsequently secrete pro-inflammatory cytokines and chemokines such as interferon gamma. Immune cells also work to initiate and potentiate chronic inflammation through the production of reactive oxygen species (ROS), and the release of molecules with degradative properties including defensins, elastase, collagenase, cathespins, and lysozyme. This long-term inflammation can lead to cell proliferation (a possible precursor to cancer), tissue remodeling, and scarring, as well as being linked to the onset of autoimmune responses in genetically disposed individuals. Chlamydia are capable of invading the majority of cultured cells, which would suggest that the receptor(s) that facilitate the invasion are either ubiquitous, or that multiple receptors are used. However, the receptor–ligand interactions involved during chlamydial entry have proven to be elusive. In addition to this, cleavage of the N-linked oligosaccharides, on the surface of C. trachomatis and C. pneumonia, inhibited attachment of the bacteria to a number of cell types, suggesting that glycan moieties of proteins expressed on the Chlamydia cell surface also participate in binding. Some of the proposed ligands that allow Chlamydia to attach to and infect host cells include the MOMP, heat shock protein 70, and glycosaminoglycans (GAGs). Studies have also shown that lipopolysaccharide (LPS), one of the major components of the chlamydial cell surface, may play a role in the infectivity of Chlamydia into host cells, although the evidence suggests that the interaction may be complex and rely on more than one moiety.
Thanks a lot! The answers are really helpful and help me understand how Chlamydia control the host! Kholhring Lalchhandama Zoheir Mellouk
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