2. Academic Validation
  3. Chlamydia psittaci plasmid-encoded CPSIT_P7 induces macrophage polarization to enhance the antibacterial response through TLR4-mediated MAPK and NF-κB pathways

Chlamydia psittaci plasmid-encoded CPSIT_P7 induces macrophage polarization to enhance the antibacterial response through TLR4-mediated MAPK and NF-κB pathways

  • Biochim Biophys Acta Mol Cell Res. 2022 Oct;1869(10):119324. doi: 10.1016/j.bbamcr.2022.119324.
Siqin He 1,  Chuan Wang 1,  Yanru Huang 1,  Simin Lu 1,  Weiwei Li 1,  Nan Ding 1,  Chaoqun Chen 2,  Yimou Wu 3
Affiliations

Affiliations

  • 1 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, China; Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China; Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang, Hunan 421001, China.
  • 2 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, China; Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China; Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang, Hunan 421001, China. Electronic address: chaoqunch@163.com.
  • 3 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, China; Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China; Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang, Hunan 421001, China. Electronic address: yimouwu@sina.com.
PMID: 35809864 DOI: 10.1016/j.bbamcr.2022.119324
Abstract

Although the protective effects of Chlamydia psittaci plasmid-encoded protein CPSIT_P7 as vaccine antigens to against chlamydial Infection have been confirmed in our previous study, the function and mechanism of CPSIT_P7 inducing innate immunity in the Antibacterial response remain unknown. Here, we found that plasmid protein CPSIT_P7 could induce M1 macrophage polarization upregulating the genes of the surface molecule CD86, proinflammatory cytokines (TNF-α, IL-6, and IL-1β), and Antibacterial effector NO Synthase 2 (iNOS). During M1 macrophage polarization, macrophages acquire phagocytic and microbicidal competence, which promotes the host Antibacterial response. As we observed that CPSIT_P7-induced M1 macrophages could partially reduce the infected mice pulmonary Chlamydia psittaci load. Furthermore, CPSIT_P7 induced M1 macrophage polarization through the TLR4-mediated MAPK and NF-κB pathways. Collectively, our results highlight the effect of CPSIT_P7 on macrophage polarization and provide new insights into new prevention and treatment strategies for chlamydial Infection.

Keywords

Antibacterial response; Chlamydia psittaci; Innate immune; MAPK; Macrophage polarization; NF-κB.

Figures
Products