Chlamydia psittaci inclusion membrane protein CPSIT_0844 elicits inflammatory IL-6 and IL-8 production in human monocytes via TLR2/TLR4 signaling pathways.

The respiratory disease caused by Chlamydia psittaci (C. psittaci) infection is often characterized by significant inflammation. In the present study, we demonstrated that the C. psittaci inclusion membrane protein CPSIT_0844 induced THP-1 cells to express IL-6 and IL-8. However, silencing of the Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) genes by using small interfering RNA (siRNA) and transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) were found to reduce the expression of IL-6 and IL-8 in THP-1 cells stimulated with CPSIT_0844. Furthermore, CPSIT_0844 induces IL-6 and IL-8 production by signaling pathways involving JNK, p38, and NF-κB in monocytes. Collectively, our findings identify CPSIT_0844 as a proinflammatory virulence factor that triggers IL-6 and IL-8 expression via a TLR2/TLR4-MyD88-dependent mechanism, culminating in the activation of MAPK and NF-κB pathways. This work provides crucial molecular insight into the inflammatory pathogenesis of C. psittaci infection.