*5.5.1 Macrophages (Mϕ)*

Macrophages (Mϕ), unlike epithelial cells, are not a hospitable niche for Chlamydial intracellular replication. Mϕs migrate to Chlamydial infection sites, phagocytose bacteria, produce proinflammatory cytokines, and destroy *C. trachomatis* with host cell autophagy [69, 70]. Also, studies have demonstrated that Mϕ autophagy can enhance antigen presentation to T-cells [69]. Furthermore, IFN-γ has been shown to enhance both autophagy and upregulation of MHC class II molecules in Mϕ [71]. Several mechanisms of *Chlamydia spp*. persistence in macrophages have been described: (1) living as aberrant RBs; (2) interaction with organelles to acquire sufficient nutrients [72, 73]; (3) modulation of inflammatory cytokines such as TNFα, IFN-γ, and ILs, to escape eradication via apoptosis or autophagy [74]; and (4) the production of adhesion molecules such as the intercellular cell adhesion molecule-1

(ICAM-1), to increase macrophage adherence, thus facilitating the migration of EBs to their preferred sites of replication [75].

Mϕs are involved in the engulfment and transient persistence of the Chlamydial extrusions [76]. Upon release from infected epithelial cells, *Chlamydia*-containing extrusions are engulfed by macrophages. Migration of these macrophages, followed by eventual escape of *Chlamydia* from them, can result in the dissemination of infectious *C. trachomatis* to more distant sites, for example, away from inflammatory foci surrounding the primary site of infection, to draining lymph nodes or to new hosts [76].

#### *5.5.2 Monocytes and dendritic cells (DC)*

Monocytes are responsible for spreading *C. trachomatis* throughout the body, while dendritic cells (DCs) play an important role in mediating immune response against bacterial infection. The *C. trachomatis* serovars Ba, D, and L2 can productively infect human peripheral blood monocytes and monocyte-derived DCs in a comparable manner [77]. *Chlamydia* Serovars Ba and D are able to persist on monocytes, while they degrade within DC's [77]. The mechanism of persistence within monocytes is not known.
