Long non‐coding RNA CRNDE and toll‐like receptor 3 correlate with disease severity, inflammation, and mortality in sepsis

Abstract

Objective This study aimed to assess the interaction between long non‐coding RNA colorectal neoplasia differentially expressed (lncRNA CRNDE) and toll‐like receptor 3 (TLR3), and assess their correlations with disease severity, inflammation, and 28‐days mortality in sepsis patients. Methods We consecutively enrolled 146 sepsis patients and 146 healthy controls (HCs), and collected their peripheral blood mononuclear cells to detect lncRNA CRNDE and TLR3 expressions using reverse transcription quantitative polymerase chain reaction. LncRNA CRNDE and TLR3 in sepsis patients were classified into four clusters according to quantile expressions (Quantile 1 (0%‐24%), Quantile 2 (25%‐50%), Quantile 3 (50%‐74%), and Quantile 4 (75%‐100%)) for correlation analysis. Results LncRNA CRNDE was upregulated in sepsis patients compared with HCs, and it showed good value in differentiating sepsis patients form HCs by receiver operating characteristic curve analysis. In sepsis patients, lncRNA CRNDE positively correlated with acute pathologic and chronic health evaluation II (APACHE II) score and sequential organ failure assessment (SOFA) score, as well as serum creatinine (Scr). As for inflammation, lncRNA CRNDE positively correlated with C‐reactive protein (CRP), tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, and IL‐8. Regarding mortality, lncRNA CRNDE positively correlated with 28‐days mortality. Furthermore, lncRNA CRNDE positively correlated with TLR3, and TLR3 positively associated with APACHE II score, SOFA score, Scr, albumin, CRP, TNF‐α, IL‐1β, IL‐6, IL‐8, and 28‐days mortality in sepsis patients. Conclusion LncRNA CRNDE interacts with TLR3, both of which correlate with advanced disease severity, inflammation, and higher 28‐days mortality in sepsis patients.

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture

“…CRANDE plays a role in tumor proliferation, migration, and the occurrence of many other diseases ( Zhou et al, 2019a ; Xie et al, 2020 ). CRANDE interacts with TLR3, and both correlate with advanced disease inflammation in sepsis patients ( Yang et al, 2020 ). The other lncRNA, OIP5-AS1, has been reported to contribute to the progression of the atherosclerosis NF-κB pathway ( Ren et al, 2020 ).…”

Long Non-Coding RNAs as Biomarkers and Therapeutic Targets in Sepsis

“…Recently, some research has showed that lncRNAs modulated sepsis by regulating different signaling pathways, such as Toll-like receptor (TLR) signaling pathway ( 34 ), which activated nuclear factor κB (NF-κB), thereby triggered inflammatory response in sepsis. A Previous study has suggested that lncRNA hox transcript antisense RNA (HOTAIR) activated the NF-κB signaling pathway to promote TNF-α expression in a murine septic model ( 35 ).…”

“…A Previous study has suggested that lncRNA hox transcript antisense RNA (HOTAIR) activated the NF-κB signaling pathway to promote TNF-α expression in a murine septic model ( 35 ). Likewise, CRNDE and NEAT1 promoted the progression of sepsis-induced injury by regulating the NF-κB signaling ( 34 , 36 ).…”

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

“…The lnc-MALAT1/miR-125a axis presents excellent value in differentiating sepsis patients from healthy controls using peripheral blood samples ( 73 ). In another study using clinical blood samples, lnc-CRNDE was found to trigger inflammation through the TLR3-NF-κB-cytokine signaling pathway and the downstream release of inflammatory cytokines ( 74 ). As a major protein related to innate immune and inflammatory responses, TLR3 is known to cause cardiac dysfunction and other organ damage during sepsis ( 74 , 75 ).…”

“…In another study using clinical blood samples, lnc-CRNDE was found to trigger inflammation through the TLR3-NF-κB-cytokine signaling pathway and the downstream release of inflammatory cytokines ( 74 ). As a major protein related to innate immune and inflammatory responses, TLR3 is known to cause cardiac dysfunction and other organ damage during sepsis ( 74 , 75 ). Low expression of lnc-MEG3 might also serve as a potential biomarker for the development, progression, and prognosis prediction of sepsis ( 76 – 78 ).…”