“…Meanwhile, the TW-183, AR-39, and TWAR strains of C. pneumoniae are the most likely to target human Mono Mac 6 cells, murine alveolar macrophages, and bone-marrow-derived macrophages (BMDMs), respectively (Beagley et al, 2009). Although it is clear that macrophages are not the optimum host cell targets for Chlamydia , owing to their powerful ability to engulf and destroy bacteria, chlamydial persistence following the infection of macrophages can be achieved through (1) the formation of aberrant RBs, to overcome imperfect conditions for growth; (2) the interaction with multiple cytoskeletons, the Golgi, and the endoplasmic reticulum, to acquire sufficient nutrients (Paradkar et al, 2008; Sun et al, 2012; Elwell et al, 2016); (3) the up- or downregulation of inflammatory mediators such as TNF-α, IFN-γ, and ILs, to escape eradication by interfering with apoptotic and autophagic pathways (Jendro et al, 2004; Sherchand et al, 2016; Chen et al, 2017); 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 (Yeung et al, 2017). The persistence of the Chlamydia spp.…”