Serum LINC01278 serves as a negative biomarker for sepsis and its up-regulation inhibits LPS-induced inflammatory response in THP-1 cells

Abstract

Background

Sepsis represents a potentially fatal condition characterized by organ failure. Long non-coding RNAs (lncRNAs) have provided new insights into the treatment of inflammation caused by sepsis.

Aims

Exploring the involvement of LINC01278 in sepsis and lipopolysaccharide (LPS)-induced inflammatory responses.

Methods

A sepsis cell model was established by stimulating THP-1 cells with LPS. Cell proliferation was assessed with the CCK-8 assay, while apoptotic cells were quantified through flow cytometric analysis. The expression of LINC01278 and miR-451a, along with the interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), were measured using RT-qPCR and ELISA, respectively. Bioinformatics tools were used to predict the targeting relationship between LINC01278 and miR-451a, and their direct interaction was validated by Dual-luciferase reporter assays and RNA immunoprecipitation (RIP).

Results

Serum LINC01278 expression was significantly lower in 108 sepsis patients than in 105 healthy controls. ROC curve and Kaplan-Meier results indicated that LINC01278 had a good diagnostic efficacy for sepsis and was negatively associated with poor prognosis. LINC01278 overexpression promoted cell viability, inhibited apoptosis, and reduced the production of IL-6, TNF-α, and IL-1β. Bioinformatics analysis identified miR-451a, which was upregulated in septic patients, as a potential target of LINC01278. Dual-luciferase reporter assays, along with RIP experiments, have verified that LINC01278 functions as a competitive endogenous RNA (ceRNA) for miR-451a.

Conclusions

LINC01278 serves as a clinical indicator for both diagnosing sepsis and assessing disease severity. LINC01278 exerts protective effects in sepsis by acting as a ceRNA for miR-451a.