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Rhodococcus equi-Derived Extracellular Vesicles Promoting Inflammatory Response in Macrophage through TLR2-NF-κB/MAPK
Zhaokun Xu1,2, Xiujing Hao1,2, Min Li1,2
1Life Science School, Ningxia University, Yinchuan 750021, China.
International Journal of Molecular Sciences
|September 9, 2022
Summary
Rhodococcus equi extracellular vesicles (EVs) trigger inflammatory responses in macrophages by activating the TLR2-NF-κB/MAPK pathways. Proteins on these EVs are responsible for this inflammatory response, impacting host-pathogen interactions.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Rhodococcus equi (R. equi) causes foal pneumonia and replicates within macrophages.
- Extracellular vesicles (EVs) from Gram-positive bacteria are virulence factors, but R. equi-EVs roles are understudied.
- Understanding R. equi-EVs interaction with host cells is crucial for elucidating pathogenicity.
Purpose of the Study:
- To investigate the properties and functions of EVs derived from virulent (103+-EVs) and avirulent (103−-EVs) R. equi strains.
- To explore the mechanisms by which R. equi-EVs induce inflammatory responses in macrophages.
- To compare the effects of EVs from virulent and avirulent R. equi strains on macrophage immune responses.
Main Methods:
- Characterization of R. equi-EVs size and morphology.
- Uptake studies of R. equi-EVs by mouse macrophage cell line J774A.1.
- Analysis of inflammatory cytokine (IL-1β, IL-6, TNF-α) expression.
- Assessment of TLR2, p-NF-κB, p-p38, and p-ERK signaling pathway activation.
- Evaluation of the effect of proteinase K-treated R. equi-EVs on macrophage responses.
Main Results:
- R. equi-EVs, similar in size to other Gram-positive EVs, were internalized by macrophages and induced cytotoxicity.
- R. equi-EVs significantly increased the expression of IL-1β, IL-6, and TNF-α in macrophages.
- Macrophage activation of TLR2, NF-κB, p38, and ERK pathways was observed upon R. equi-EVs stimulation.
- Proteinase K treatment of R. equi-EVs abolished the inflammatory response and pathway activation, indicating the role of EV proteins.
Conclusions:
- R. equi-derived EVs mediate inflammatory responses in macrophages via the TLR2-NF-κB/MAPK signaling pathways.
- Proteins on R. equi-EVs are the key mediators of these inflammatory responses.
- This study provides the first insights into the role of R. equi-EVs in host immune responses and highlights differences between virulent and avirulent strains, advancing understanding of R. equi pathogenicity.
