**2.5 Chlamydial cryptic plasmid**

The removal of the chlamydial cryptic plasmid in the murine equivalent model of *C. trachomatis, C. muridarum*, has led to reduced bacterial load and upper genital tract and ocular pathologies [1]. The possible mechanisms include the action of two plasmid genes involved in the formation of the antigen Pgp3, a secreted protein component of the outer plasmid membrane, and Pgp4 which is a regulator of both plasmid and chromosomal genes [1]. The products of these genes are related to glycogen production and accumulation, a contributor to virulence [9, 18]. Pgp4 acts also as a transcriptional regulator of both plasmid and chromosomal virulenceassociated genes [18]. Both *pgp3* and *pgp*4 genes are essential for in vitro growth of

the bacterium, which enforces the aspect that their products are virulence factors [18]. This aspect is enforced by the fact that *pgp*4 is expressed only three hours postinfection [10, 18]. In mice, pGP3 promotes ascending infection and tubal inflammation. The mechanism seems to be via neutralizing the host antimicrobial peptides, like human alpha-defensins, human neutrophil peptide 2, human beta-defensin 3, and cathelicidin LL-37. Host antimicrobial peptides are trapped by pGP3 to form stable complexes. In this way the progeny Elementary Bodies released can safely evade the next host cell [20]. The plasmid-encoded protein CPSIT\_P7 of *C. psittaci* via Toll-like receptor 4 and TLR4/Mal/MyD88/NF-κB signaling axis, triggers the expression of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 [21].

#### **2.6 Protein CT135**

Protein CT135 is responsible for persistent urogenital infection in mice and prolonged time to clearance in vivo [1].
