Polymorphisms in Chlamydia trachomatis tryptophan synthase genes differentiate between genital and ocular isolates

A characteristic of polymorphic membrane protein F of Chlamydia trachomatis isolated from male urogenital tracts in Japan

“…showing that in contrast to ocular strains vaginal microbial flora could allow C. trachomatis urogenital strains to escape IFN-gamma-mediated eradication and establish persistent infection [18,22], is supporting our speculation. In addition, since it has been reported that…”

Chlamydophila pneumoniae in human immortal Jurkat cells and primary lymphocytes uncontrolled by interferon-γ

“…The effect of IFN- effect on chlamydial elimination in human epithelial cells is responsible for IDO induction [9][10][11][12][13][14]; therefore, we next assessed whether gene expression of IDO could be induced by IFN- in Jurkat cells. As shown in Fig.…”

“…Interferon (IFN)- inhibits the replication of pathogenic chlamydiae in human cells by inducing the production of the enzyme indoleamine 2,3-dioxygenase (IDO), resulting in depletion of tryptophan in infected cells, which is an essential amino acid for intracellular growth of pathogenic chlamydiae [9][10][11]. Therefore, induction of IDO is the most important antichlamydial factor in humans, induced by IFN-, and moreover, human-adapted chlamydiae have specifically coevolved with their host to circumvent the effect of IFN- [9][10][11].…”

“…Therefore, induction of IDO is the most important antichlamydial factor in humans, induced by IFN-, and moreover, human-adapted chlamydiae have specifically coevolved with their host to circumvent the effect of IFN- [9][10][11]. In fact, IFN- induces C. pneumoniae persistent infection, characterized by an absence of culturability [12][13][14], altered bacterial RNA and protein levels [6], and morphologically altered chlamydial bodies [12][13][14], with an uncompleted developmental cycle and inhibition of elementary body maturation, followed by 5 bacterial elimination [12][13][14].…”

“…trachomatis A-C serotypes), encode a functional tryptophan synthetase enzyme (trpAB), which possibly uses exogenous indole supplied from microbes that colonize the human genital tract [9]. Therefore, they can survive in genital cells, even in the presence of IFN-, which is directly related to recurrent infection by Ch.…”