**2.7 Silencing the NF-κB inflammatory pathway**

*Chlamydiae* seem to suppress NF-κB activation in infected cells. This is in contrast with the production of proinflammatory cytokines that are induced during infection. It appears that the microbe activates MAP kinases in its favor to acquire the needed nutrients for survival. The mechanism seems to be cleavage of NF-κB p65 into the fragments p40 and p20 by a chlamydial protein called tail-specific protease. The overexpression of p40 leads to interaction of the fragment with the cytoplasmic inhibitor of NF-κB I-κBα and blockage of NF-κB pathways [13]. SINC protein of *C. psittaci* targets the inner nuclear membrane of infected host cells. As a result, it is involved in controlling of nuclear structure and gene silencing [7, 22].

#### **2.8 Translocated actin recruiting protein (TarP)**

Upon attachment of the elementary body to the host cell, TarP is injected into the host cell. This translocation is made via a chlamydial type 3 secretory system. TarP has three binding sites for vinculin [23]. Additionally, TarP is reported to interact with focal adhesion kinase (FAK) and thus be able to alter cell adhesion signaling [23]. In this way, *Chlamydiae* use extracellular matrix and cell-to-cell junction for their benefit to promote entry to the host cells [23].

#### **2.9 Chlamydial polymorphic outer membrane proteins (Pmps)**

Chlamydial polymorphic outer membrane proteins are surface proteins that serve as adhesins, but also have antigenic role. They are present in all chlamydial species. They act as autotransporters that is they can translocate. These proteins are considered virulence factors. *Chlamydia*e in contrast to other Gram-negative bacteria possess more autotransporter proteins. PmpB, C, D, and I of *C. trachomatis* are known to induce strong humoral immune responses in infected patients. Women patients suffering from pelvic inflammatory disease and proved positive for anti-PmpA specific antibodies had a significantly high infertility rate in comparison to women negative for anti-PmpA antibodies. *C. pneumonia* Pmp20 and Pmp21 induce IL-6 and monocyte chemoattractant protein-1 production in human umbilical vein endothelial cells (HUVECs) by activation of NF-kB. The production is dose-dependent and the

two Pmps do not act synergistically. *C. trachomatis* PmpD induces strong and dosedependent IL-8 production from the human monocyte cell line THP-1 [10, 24].
