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Updated: Jun 15, 2025

Intravitreal Injection and Quantitation of Infection Parameters in a Mouse Model of Bacterial Endophthalmitis
Published on: February 6, 2021
miR-27a-3p promotes inflammatory response in infectious endophthalmitis via targeting TSC1
Yanting Chen1, Shanxiang Li2, Hong He2
1Hainan Eye Hospital and Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, No.19 Xiuhua Road, Xiuying District, Haikou, 570311, Hainan, China. bery1455@126.com.
Abstract:
Infectious endophthalmitis (IE) poses a significant threat to vision. This study aimed to explore the impact of microRNA (miR)-27a-3p on inflammation in IE. A rat model was developed through intravitreal injection of lipopolysaccharide. Clinical and demographic data were collected for 54 participants: 31 diagnosed with IE and 23 non-infectious patients with idiopathic macular holes. Expression levels of miR-27a-3p and inflammatory genes were quantified via reverse transcription quantitative polymerase chain reaction. Concentrations of inflammatory cytokines in human vitreous samples were measured using enzyme-linked immunosorbent assay. In vitro studies were conducted to explore the target gene of miR-27a-3p. The final animal experiments further verified the role of miR-27a-3p and tuberous sclerosis complex (TSC)1 in inflammatory responses. Results showed that miR-27a-3p was elevated in LPS-treated rats and IE patients. Thirty-one IE patients were divided into the High (n = 15) and Low (n = 16) groups according to the expression of miR-27a-3p. No significant differences were observed in baseline clinical and demographic characteristics between the control and IE patient groups. Pro-inflammatory cytokine mRNA levels and concentrations were notably increased in both LPS-treated rats and the High group of patients. Besides, results showed that TSC1 is a target gene of miR-27a-3p. Moreover, TSC1 inhibition promoted inflammation in rat vitreous samples. In summary, our findings suggested that miR-27a-3p exacerbated inflammatory responses in IE though targeting TSC1, offering novel insights for potential therapeutic strategies targeting miR-27a-3p in the clinical management of IE.
Insights
MicroRNA-27a-3p worsens inflammation in infectious endophthalmitis (IE) by targeting TSC1. This finding offers new therapeutic strategies for IE management.
Area of Science:
- Ophthalmology
- Molecular Biology
- Immunology
Background:
- Infectious endophthalmitis (IE) is a severe ocular condition that threatens vision.
- MicroRNAs (miRNAs) play crucial roles in regulating inflammatory processes.
- The specific role of microRNA (miR)-27a-3p in IE pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the impact of miR-27a-3p on inflammation in infectious endophthalmitis (IE).
- To identify the target gene of miR-27a-3p involved in IE-related inflammation.
- To explore the potential of targeting miR-27a-3p for IE therapeutic strategies.
Main Methods:
- Established a rat model of IE using intravitreal lipopolysaccharide (LPS) injection.
- Quantified miR-27a-3p and inflammatory gene expression using RT-qPCR in rats and human samples.
- Measured inflammatory cytokine concentrations in human vitreous samples via ELISA and conducted in vitro studies to identify miR-27a-3p targets.
Main Results:
- miR-27a-3p levels were significantly elevated in LPS-treated rats and IE patients compared to controls.
- Patients with higher miR-27a-3p expression exhibited increased pro-inflammatory cytokine levels.
- Tuberous sclerosis complex 1 (TSC1) was identified as a direct target gene of miR-27a-3p, and its inhibition promoted inflammation.
Conclusions:
- miR-27a-3p exacerbates inflammatory responses in infectious endophthalmitis (IE) through targeting TSC1.
- Elevated miR-27a-3p is a potential biomarker for IE severity.
- Targeting miR-27a-3p presents a promising therapeutic avenue for managing IE.
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