trachomatis inclusions (Coers et al , 2008) This localization wa

trachomatis inclusions (Coers et al., 2008). This localization was observed only with C. trachomatis, while C. muridarum seems to have evolved mechanisms that prevent the accumulation of GTPases in the chlamydial inclusion, a possible immune evasion strategy (Coers et al., 2008). Although most of the assessed pathways seem to help the host cell in bacterial clearance, there is evidence that Chlamydiales also use TLRs to establish a replication-friendly environment. Chlamydia pneumoniae raises ATP levels through activation of the TLR2/Myd88 pathway. This behavior is crucial

because Chlamydiales are unable to produce ATP (Yaraei et al., 2005). MIP-2 and KC are two chemokines expressed upon Myd88 BI 6727 clinical trial activation. In infected mice, these chemokines attract polymorphonuclear neutrophils to the lungs. Chlamydia pneumoniae is thought to use these cells to spread Target Selective Inhibitor Library throughout the lungs (Rodriguez et al., 2005). Immune cells can therefore be used as vehicles to reach new tissues instead of fighting the infection. Interaction of Chlamydiales with TLRs is of particular interest because they control inflammation that can become chronic or, if uncontrolled, cause damage. For example,

TLR2 recognition of bacterial PAMPs was linked to trophoblast apoptosis (Abrahams et al., 2004), which could provoke preterm delivery. Similarly, exposure to chlamydial Hsp60 (CHsp60) induces apoptosis in trophoblasts. Trophoblast TLR4 recognized CHsp60 and, through an unknown signaling pathway, induced several downstream caspases (Equils et al., 2006). Development of atherosclerosis was reduced in TLR2-deficient mice infected with C. pneumoniae. Without the TLRs, the level of circulating cytokines

was reduced and less dendritic cells were activated these (Naiki et al., 2008). Thus, different yet unknown chlamydial antigens seem to induce such a strong response that they cause severe damage to the surrounding tissue. Downstream of PRRs, there are not only cytokines and their receptors but also several enzymes that synthesize microbicidal molecules. ROS are strong microbicidals produced by macrophages, dendritic cells and neutrophils. Most of them are produced by NADPH oxidase (Nox), a multiproteic transmembrane complex. This family of genes is found only in multicellular organisms, with few exceptions (reviewed in Bedard & Krause, 2007). There are three different classes of NADPH oxidases (reviewed in Bedard et al., 2007). In most mammals, all seven genes are found, while rodents lack Nox5. The Nox present in phagocytic cells is Nox2. It is not clear whether other members of the Nox family are also specifically induced upon infection of phagocytic cells. Chronic granulomatous disease is a severe and debilitating disease found in individuals with mutations in components of the Nox2 complex.

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