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Chlamydia psittaci hypothetical inclusion membrane protein CPSIT_0842 evokes a pro-inflammatory response in monocytes
Jian Xiao1, Jun He2, Zhangping He1
1Institute of Pathogenic Biology, Hengyang Medical College, University of South China; Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hengyang, Hunan, 421001, China; The Affiliated Nanhua Hospital, Department of laboratory medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China; Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, Hunan, 421001, China.
Abstract:
Chlamydia psittaci (C. psittaci) is an obligate intracellular pathogen that resides within a membrane-bound compartment known as the inclusion. Upon entering the host cell, Chlamydiae secrete numerous proteins to modify the inclusion membrane. Inclusion membrane (Inc) proteins are important pathogenic factors in Chlamydia and play crucial roles in the growth and development of Chlamydia. In the present study, the C. psittaci protein, CPSIT_0842, was identified and shown to localize to the inclusion membrane. Temporal analysis revealed that CPSIT_0842 is an early expression protein of Chlamydia. Moreover, this protein was shown to induce the expression of pro-inflammatory cytokines IL-6 and IL-8 in human monocytes (THP-1 cells) via the TLR2/TLR4 signaling pathway. CPSIT_0842 increases the expression of TLR2, TLR4, and adaptor MyD88. Suppression of TLR2, TLR4, and MyD88 markedly attenuated CPSIT_0842-induced production of IL-6 and IL-8. MAP kinases and NF-κB, important downstream molecules of TLR receptors in inflammatory signaling pathways, were also confirmed to be activated by CPSIT_0842. CPSIT_0842-induced production of IL-6 was reliant on activation of the ERK, p38, and NF-κB signaling pathways while IL-8 expression was regulated by the ERK, JNK, and NF-κB signaling pathways. Specific inhibitors of these signaling pathways significantly decreased CPSIT_0842-mediated expression of IL-6 and IL-8. Together these findings demonstrate that CPSIT_0842 upregulates the expression of IL-6 and IL-8 via TLR-2/TLR4-mediated MAPK and NF-κB signaling pathways in THP-1 cells. Exploring these molecular mechanisms enhances our understanding of C. psittaci pathogenesis.
Insights
Chlamydia psittaci protein CPSIT_0842 triggers inflammation by boosting IL-6 and IL-8 production in human monocytes. This occurs through Toll-like receptor 2/4 (TLR2/TLR4) and downstream signaling pathways, revealing a key mechanism in C. psittaci pathogenesis.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Chlamydia psittaci (C. psittaci) is an obligate intracellular bacterium.
- C. psittaci modifies host cells using inclusion membrane (Inc) proteins.
- Understanding Inc proteins is crucial for C. psittaci pathogenesis.
Purpose of the Study:
- Identify and characterize C. psittaci protein CPSIT_0842.
- Investigate CPSIT_0842's role in host inflammatory responses.
- Elucidate the molecular pathways involved in CPSIT_0842-induced inflammation.
Main Methods:
- Localization and temporal expression analysis of CPSIT_0842.
- Stimulation of human THP-1 monocytes with CPSIT_0842.
- Assessment of cytokine (IL-6, IL-8) production.
- Analysis of Toll-like receptor (TLR2/TLR4), MyD88, MAP kinase, and NF-κB signaling pathways.
Main Results:
- CPSIT_0842 localizes to the inclusion membrane and is an early expressed protein.
- CPSIT_0842 induces IL-6 and IL-8 production in THP-1 cells.
- CPSIT_0842 upregulates TLR2, TLR4, and MyD88 expression.
- Activation of MAPK (ERK, p38, JNK) and NF-κB pathways by CPSIT_0842.
- Inhibition of these pathways attenuates cytokine production.
Conclusions:
- CPSIT_0842 is an early C. psittaci protein that promotes inflammation.
- The TLR2/TLR4-mediated activation of MAPK and NF-κB pathways is critical for CPSIT_0842-induced IL-6 and IL-8 production.
- These findings provide insights into C. psittaci pathogenesis and host immune response.
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