Using the mouse model, it has been well demonstrated that chlamydia respiratory infections during early life modify lung physiology where it increases the severity of allergic airway disease by targeting factor like interleukin-13 (IL-13) (Starkey et al., 2013[30]) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) (Starkey et al., 2014[32][31]). This evidence concerns the gene IL13 and chlamydia trachomatis infectious disease.