Chlamydia psittaci plasmid-encoded CPSIT_P7 induces macrophage polarization to enhance the antibacterial response through TLR4-mediated MAPK and NF-κB pathways.
Antibacterial response
Chlamydia psittaci
Innate immune
MAPK
Macrophage polarization
NF-κB
Journal
Biochimica et biophysica acta. Molecular cell research
ISSN: 1879-2596
Titre abrégé: Biochim Biophys Acta Mol Cell Res
Pays: Netherlands
ID NLM: 101731731
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
28
03
2022
revised:
23
06
2022
accepted:
30
06
2022
pubmed:
10
7
2022
medline:
10
8
2022
entrez:
9
7
2022
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 35809864
pii: S0167-4889(22)00116-1
doi: 10.1016/j.bbamcr.2022.119324
pii:
doi:
Substances chimiques
Anti-Bacterial Agents
0
NF-kappa B
0
Tlr4 protein, mouse
0
Toll-Like Receptor 4
0
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
119324Informations de copyright
Copyright © 2022 Elsevier B.V. All rights reserved.