Evidence map›Paper›PMID 40879870›Full record

ArticleMolecular biology reports2025

miR-155 aggravates inflammation in MRSA pneumonia by modulating macrophage polarization.

Yunfeng Shi, Xiaohan Shi, Yang Yang, Xiaona Lin, Yuhang Pan, Benquan Wu

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yunfeng Shi *Department of Medical Intensive Care Unit, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Xiaohan Shi *Department of ICU, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Zhejiang, China.
Yang YangDepartment of Medical Intensive Care Unit, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Xiaona LinThe First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China.
Yuhang PanDepartment of Pathology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Benquan WuDepartment of Medical Intensive Care Unit, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. zswbq@163.com.

Funding

National Natural Science Foundation of China 81170004
6 · The paper itself

Abstract

backgroundMethicillin-resistant Staphylococcus aureus (MRSA) pneumonia is a severe infection with high mortality, where alveolar macrophages (AMs) play a critical role in host defense through M1 polarization. MicroRNA-155 (miR-155) is known to modulate immune responses, but its specific role in AM polarization during MRSA pneumonia remains unclear. This study investigates how miR-155 regulates M1 macrophage polarization and MRSA pneumonia.

methodsThe experiments were performed in both vitro and in miR-155 knockout mice. The activity of miR-155 and polarization of AMs were evaluated using scanning electron microscopy, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Lung pathology, inflammatory markers, and potential signaling pathways (particularly AKT/mTOR) were analyzed.

resultsmiR-155 expression was significantly upregualted in MRSA infection, while miR-155 promoted M1 macrophage polarization as demonstrated by distinct morphological changes, elevated CD86 levels, and increased IL-6 production. miR-155 deficiency attenuated this response, reducing inflammatory cytokine release and lung pathology while impairing AKT/mTOR pathway activation, indicating that miR-155 exacerbates MRSA-induced pneumonia by driving M1 polarization through AKT/mTOR signaling.

conclusionsOur findings reveal that miR-155 modulates M1 macrophage polarization and aggrevates MRSA-induced pneumonia by activating the AKT/mTOR pathway. This study provides new insights into host-pathogen interactions in MRSA infection, suggesting miR-155 as a potential therapeutic target.

Indexed as

Macrophages, AlveolarMethicillin-Resistant Staphylococcus aureusMicroRNAsPneumoniaPneumonia, StaphylococcalAnimalsCell PolarityInflammationMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteins c-aktSignal TransductionStaphylococcal InfectionsMicroRNAsMirn155 microRNA, mouseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAcute pneumoniaMacrophageMethicillin resistant staphylococcus aureusMicroRNA 155Polarization

Identifiers

PMID40879870

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