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miR-325-3p targets GSDMD in macrophages to attenuate lung injury induced by Streptococcus equi subsp. zooepidemicus
Yajuan Li1, Li Jiang2, Qiuguo Fang2
1School of Animal Science and Technology, Foshan University, Foshan, Guangdong 528225, China; Foshan University Veterinary Teaching Hospital, Foshan University, Foshan 528225, China.
Abstract:
Streptococcus equi subsp. zooepidemicus (SEZ) primarily functions as a zoonotic pathogen, with the capacity to infect a wide variety of animal species, including humans. The present study has captured the importance role of GSDMD in mice against SEZ, here, with the help of published works, we chose miR-325-3p as a regulator to GSDMD and investigated the role of miR-325-3p during SEZ infection in vitro and vivo. In this study, SEZ significantly increased the expression of GSDMD and release of cytokines in macrophages. Both prediction assay using Target Scan databases and luciferase reporter assay showed that miR-325-3p directly targeted to GSDMD. Moreover, overexpression of miR-325-3p significantly decreased the expression of GSDMD and the release of IL-1β and IL-18 in macrophages infected with SEZ. And inhibition of miR-325-3p expression exhibited the opposite effect. In vivo experiments, we found that injection of miR-325-3p mimics into mice alleviated lung injury induced with SEZ, and miR-325-3p mimics also reduced the IL-1β and IL-18 contents in bronchoalveolar lavage fluid (BALF) and bacterial loads in lung tissue. Results in this study revealed that miR-325-3p suppressed inflammatory response triggered by SEZ both in vitro and vivo. Taken together, our findings provided evidence to identify miR-325-3p as a potential therapeutic agent to SEZ infection.
Insights
MicroRNA-325-3p regulates GSDMD, reducing inflammation and lung injury caused by Streptococcus equi subsp. zooepidemicus (SEZ) infection in mice. This study identifies miR-325-3p as a potential therapeutic for SEZ infections.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Streptococcus equi subsp. zooepidemicus (SEZ) is a zoonotic pathogen causing infections in various species, including humans.
- Gasdermin D (GSDMD) plays a crucial role in the inflammatory response during SEZ infection.
- MicroRNAs (miRNAs) are key regulators of gene expression and inflammatory pathways.
Purpose of the Study:
- To investigate the role of miR-325-3p as a regulator of GSDMD in the context of SEZ infection.
- To evaluate the therapeutic potential of miR-325-3p against SEZ-induced inflammation and lung injury.
Main Methods:
- In vitro studies using macrophages infected with SEZ.
- In vivo experiments involving SEZ-infected mice treated with miR-325-3p mimics.
- Bioinformatic prediction (Target Scan) and luciferase reporter assays to confirm miRNA-target interaction.
- Measurement of GSDMD expression, cytokine release (IL-1β, IL-18), lung injury, and bacterial load.
Main Results:
- SEZ infection increased GSDMD expression and cytokine release in macrophages.
- miR-325-3p directly targets GSDMD.
- Overexpression of miR-325-3p suppressed GSDMD, IL-1β, and IL-18 release in vitro.
- In vivo, miR-325-3p mimics reduced lung injury, inflammation (IL-1β, IL-18 in BALF), and bacterial load in SEZ-infected mice.
Conclusions:
- miR-325-3p effectively suppresses the inflammatory response triggered by SEZ infection.
- miR-325-3p demonstrates therapeutic potential for treating SEZ infections by modulating GSDMD.
- This study highlights miR-325-3p as a promising therapeutic agent against SEZ-induced pathology.
