PubMedCrossRef 71. Joubert O, Keller D, Pinck

A, Monteil H, Prevost G: Sensitive and specific detection of staphylococcal epidermolysins A and B in broth cultures by flow cytometry-assisted multiplex immunoassay. J Clin Microbiol 2005, 43:1076–1080.PubMedCrossRef Competing interests Authors declare no conflict of interest. Authors’ contributions Conception and design of the study: LB-M and GP. Acquisition of data: HS, AT-A, WM, YB, HB. Analysis and interpretation of data: LB, GP, YS. Drafting the article: LB-M, SOK, and HS. Revising it critically for important intellectual content: LB-M, GP, SOK, YS. Final approval of the version to be submitted: All the co-authors. All authors read and approved the final manuscript.”
“Background Chlamydia trachomatis causes sexually transmitted infections and is the leading cause of preventable blindness worldwide [1]. Chlamydia are Gram-negative, obligate intracellular bacteria with a unique, biphasic check details developmental cycle that takes place in a membrane-bound vacuole termed the inclusion. The infectious but metabolically inactive elementary body (EB) attaches to epithelial cells and initiates its uptake through parasite mediated S63845 concentration endocytosis [2]. Once internalized, EBs differentiate into

metabolically active but non-infectious reticulate bodies (RBs) which replicate by binary fission. As the infection progresses, RBs differentiate into EBs in an asynchronous manner and these infectious EBs are eventually released into the host to initiate a additional rounds of infection. Following infection, the inclusion membrane is modified through the insertion of multiple bacterial type three secreted effector proteins [3]. These inclusions are non-fusogenic with the endosomal and lysosomal pathways [4]. Inclusions are trafficked along microtubules in a dynein-dependent manner to the microtubule organizing center (MTOC) where they intercept host-derived lipids to maintain the integrity of the expanding inclusion [5]. Thus, despite being sequestered within a membrane-bound vacuole, chlamydiae

manipulate the host and subvert Montelukast Sodium host pathways to establish an environment that is not only conducive to replication and differentiation but also simultaneously protected from host immune responses. At high multiplicities of infection, multiple inclusions fuse into a single inclusion. This fusion event is critical for pathogenicity; rare isolates with non-fusogenic inclusions are clinically associated with less severe signs of infection and lower numbers of recoverable bacteria than wild-type isolates [6]. Inclusion fusion occurs even between different C. trachomatis serovars potentially facilitating genetic exchange between serovars [7]. Previous studies have demonstrated that the fusion of chlamydial inclusions requires bacterial protein synthesis and is inhibited during growth at 32°C [8]. Specifically, the inclusion membrane protein IncA is required for the homotypic fusion of chlamydial inclusions [9].