The dual role of cytokine responses to Chlamydia trachomatis infection in host pathogen crosstalk.

Chlamydia-induced diseases are a significant human health disease. In recent years, a large number of studies have helped to gradually improve our understanding of chlamydia. For example, in the lifestyle of a parasitic host, chlamydia infection stimulates T cell and macrophage-mediated immune responses in the host. Different immune cells produce different cytokines and different immune effects. Th1 cells produce IL-2, IL-12, and IFN-γ, while Th2 cells produce IL-4 and IL-10. The two cytokines produced by T cells play different roles when chlamydia infects the host. In which immune link are these cytokines produced and what role do they play after production? Understanding these mechanisms of action, will help us to develop new strategies against problems caused by chlamydia. Chlamydia trachomatis infection often shows persistence and repeatability due to the lack of bactericidal immunity in humans. The consequences of persistent chlamydia infection can be severe, and can include salpingitis and follicular conjunctival scarring. Recently, many studies have suggested that chlamydia-induced changes in inflammation can affect humans and animals to varying degrees. It is important to study the ways in which these changes can influence the mammalian hosts. Herein, we investigated changes in cytokine expression following chlamydial infection, how this affects disease pathogenesis in chlamydia, and we use this to understand the cause of the high recurrence rate after chlamydial infection. In addition, we summarize the different cytokines produced by other immune cells after chlamydia infection, emphasizing the interaction between various cytokines. Finally, we outline how to deal with the duality of cytokines and reduce their adverse effects after protoplasmic infection.