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PubMed: 38834979 DOI: 10.1186/s12865-024-00624-0

miR-486-5p predicted adverse outcomes of SCAP and regulated K. pneumonia infection via FOXO1.

BMC Immunol 25(1):33

Authors: Qianqi Jin, Chuanlan Liu, Yan Cao, Feiyan Wang

Affiliations

  • Department of Clinic Laboratory, The Sixth Hospital of Wuhan Affiliated Hospital of Jianghan University, Wuhan, 430015, China.
  • Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry, Sichuan Engineering Laboratory for Plant-Sourced Drug, and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu, 610041, China.
  • Department of Emergency Medical, Shanghai Sixth People's Hospital, No. 600, Yishan Road, Xuhui District, Shanghai, 200233, China.
  • Department of Emergency Medical, Shanghai Sixth People's Hospital, No. 600, Yishan Road, Xuhui District, Shanghai, 200233, China.

Abstract

PURPOSE

Severe community-acquired pneumonia (SCAP) is a common respiratory system disease with rapid development and high mortality. Exploring effective biomarkers for early detection and development prediction of SCAP is of urgent need. The function of miR-486-5p in SCAP diagnosis and prognosis was evaluated to identify a promising biomarker for SCAP.

PATIENTS AND METHODS

The serum miR-486-5p in 83 patients with SCAP, 52 healthy individuals, and 68 patients with mild CAP (MCAP) patients were analyzed by PCR. ROC analysis estimated miR-486-5p in screening SCAP, and the Kaplan-Meier and Cox regression analyses evaluated the predictive value of miR-486-5p. The risk factors for MCAP patients developing SCAP were assessed by logistic analysis. The alveolar epithelial cell was treated with Klebsiella pneumonia to mimic the occurrence of SCAP. The targeting mechanism underlying miR-486-5p was evaluated by luciferase reporter assay.

RESULTS

Upregulated serum miR-486-5p screened SCAP from healthy individuals and MCAP patients with high sensitivity and specificity. Increasing serum miR-486-5p predicted the poor outcomes of SCAP and served as a risk factor for MCAP developing into SCAP. K. pneumonia induced suppressed proliferation, significant inflammation and oxidative stress in alveolar epithelial cells, and silencing miR-486-5p attenuated it. miR-486-5p negatively regulated FOXO1, and the knockdown of FOXO1 reversed the effect of miR-486-5p in K. pneumonia-treated alveolar epithelial cells.

CONCLUSION

miR-486-5p acted as a biomarker for the screening and monitoring of SCAP and predicting the malignancy of MCAP. Silencing miR-486-5p alleviated inflammation and oxidative stress induced by K. pneumonia via negatively modulating FOXO1.

MeSH

Cells, Alveolar Epithelial Cells, Serum, Epithelial Cells, Stress, Physiological, Oxidative Stress, Biomarkers, Pneumonia, Immune System, Risk Factors, Infections

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