All authors approved the final manuscript.”
“Background Chlamydia trachomatis is an obligate intracellular pathogen with unique biphasic developmental cycle alternating between the infectious elementary selleck chemical body (EB) and the metabolically active reticulate body (RB). Based on the antigenic variation of the major outer membrane GDC 0032 clinical trial protein (MOMP), the C. trachomatis isolates have been divided into three different biovariants [1]. Serovars A, B, Ba and C cause ocular

infections, currently infecting 150 million people worldwide [2,3]; serovars D, E, F, G, H, I, J and K cause sexually transmitted disease with more than 90 million new cases of genital infections occurring every year [4,5] and serovars L1, L2 and L3 cause lymphgranuloma

venereum (LGV) primarily affecting the lymphatic system with recent outbreaks in Western Europe [6,7]. Comparative genomic studies demonstrate that the genome of C. trachomatis serovars are strikingly similar to each other find more and share more than 99% identity [8,9]. Genetic differences were observed centring around the plasticity zone i.e. ~50 kb region near the predicted termination origin of the genome, experiencing a higher degree of DNA arrangement [10], MOMP and members of polymorphic membrane protein (pmp) gene family [11]. However the occurrence of quantitatively different infections by different serovars within a given host has been intriguing. In vivo studies infecting mice intranasally [12] or intravaginally [13] with different serovars of C. trachomatis has revealed a great deal of variation in infection kinetics.

Genome analysis could reveal that a functional tryptophan synthase enzyme and toxin might be the principal virulence factors underlying this distinct tropism in terms of organ specific disease termed as organotropism [14]. Studies including LGV serovars confirmed the observation that the variability resided mainly in the plasticity zone [15]. Chlamydia primarily targets the host epithelial cells and resides within distinct membrane bound vacuoles termed as chlamydial inclusion. The chlamydia proliferate within inclusion and inhibits their acidification by Y-27632 2HCl avoiding fusion with lysosomal compartments [16,17]. However the association of C. trachomatis with reactive arthritis have raised questions how chlamydia is transported from the site of infection to the site of inflammatory disease in the joints or vasculature [18-20]. Studies have shown that the C. trachomatis infection is characterized by infiltration with polymorphonuclear leukocyte (PMNs) in the acute phase and mononuclear cells in the chronic phase [21]. Hence there have been suggestions that circulating monocytes delivers the pathogen to other organs and initiate immunological response and inflammation. The role of C.