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.

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Publication Details

Journal
Immunobiology
Published
2026-01-20
DOI
https://doi.org/10.1016/j.imbio.2026.153160
Primary Topic
Reproductive tract infections research
Type
article
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article

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

Buwei Wang, Xiaoliang Yan, Kang Zheng, Yuqing Chen et al.
Immunobiology
Reproductive tract infections research
article

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

Buwei Wang, Xiaoliang Yan, Kang Zheng, Yuqing Chen, Yimou Wu, Chuan Wang, Zhangping He, Yating Wen, Dan Luo, Yumeng Li, Jian Xiao
article en

Abstract

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.

ImmunobiologyVol. 231(2)
Hengyang Normal University (CN), Xiangyang Central Hospital (CN), Hengyang Academy of Agricultural Sciences (CN), University of South China (CN)
Good health and well-being
Openalex Percentile: Top 83%
Reproductive tract infections research
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Chlamydia psittaci inclusion membrane protein CPSIT_0844 elicits inflammatory IL-6 and IL-8 production in human monocytes via TLR2/TLR4 signaling pathways — Buwei Wang, Xiaoliang Yan, et al. · Immunobiology (2026) | TGRS Research Map | TGRS