Abstract
BackgroundThis present study aimed to investigate the correlation of long non‐coding RNA THRIL (lnc‐THRIL) with acute respiratory distress syndrome (ARDS) risk, disease severity, inflammation, and mortality in sepsis patients.MethodsA total of 109 sepsis patients admitted to intensive care units were consecutively recruited, and their blood samples were collected. After admission, patients were supervised and screened daily to identify the occurrence of ARDS. Clinical characteristics, routine laboratory testing, and disease severity were recorded, and all enrolled patients were followed up until death in the hospital or discharge for mortality records. Lnc‐THRIL was detected by quantitative polymerase chain reaction, and inflammatory cytokine levels were measured by human enzyme‐linked immunoassay.ResultsA total of 32 (29.4%) sepsis patients occurred ARDS and 77 (71.6%) did not. Lnc‐THRIL was upregulated in ARDS group compared with non‐ARDS group, and it had good value in distinguishing ARDS from non‐ARDS in sepsis patients (AUC: 0.706; 95%CI: 0.602‐0.809). Besides, lnc‐THRIL, smoke, and chronic obstructive pulmonary disease independently predicted increased risk of ARDS. As for disease severity, lnc‐THRIL positively correlated with APACHE II score and SOFA score in sepsis patients. Regarding inflammation, lnc‐THRIL was positively associated with CRP, PCT, TNF‐α, and IL‐1β levels in sepsis patients. Additionally, the mortality rate was 30.2%, and lnc‐THRIL was upregulated in non‐survivors compared with survivors, presenting a good value (AUC: 0.780; 95%CI: 0.683‐0.876) in predicting mortality in sepsis patients.ConclusionLnc‐THRIL predicts increased risk of ARDS and positively correlates with disease severity, inflammation, and mortality in sepsis patients.
Highlights
Sepsis is defined as life‐threatening organ dysfunction resulted from dysregulated host immune response and systemic inflammation to microbial infection.[1]
We observed that: (a) 29.4% of sepsis pa‐ tients developed acute respiratory distress syndrome (ARDS) during hospitalization, and lnc‐THRIL independently predicted increased risk of ARDS; (b) lnc‐THRIL was positively correlated with disease severity and inflammatory
As one of the novel Long non‐coding RNA (lncRNA), lnc‐THRIL is initially disclosed to regulate the expression of Tumor necrosis factor (TNF)‐α, which is a key mediator of inflammation and immune response by forming a complex with heterogeneous nuclear ribonucleoprotein L (hnRNPL) and binding to the promoter region of TNF‐α, and it influences the expression of inflammatory cytokines such as IL‐1β, IL‐6, and IL‐8.9,11 lnc‐THRIL is reported to influence inflammation‐related cell injuries in inflammatory diseases, and cell injury, especially alveolar epithelial cells injury that is one of the main contributors for the development of ARDS in sepsis.[11,12]
Summary
Sepsis is defined as life‐threatening organ dysfunction resulted from dysregulated host immune response and systemic inflammation to microbial infection.[1]. It is estimated to influence more than 19 mil‐ lion people each year globally, and the in‐hospital mortality rates are around 15%‐25% for sepsis patients.[2,3]. Pulmonary dysfunction such as acute respiratory distress syndrome (ARDS) is one of the predominant organ dysfunctions caused by systemic inflammation, uncontrolled cytokine, or release of other mediators, which contributes to the high mortality of sepsis and reduces the qual‐ ity of life for sepsis survivors.[4,5]. The function of lnc‐THRIL in sepsis (a typical immune response‐induced inflammatory disease) or its correlation with ARDS in sepsis patients is still not clear. We hypothesized that lnc‐THRIL might participate in the pathogenesis of sepsis and contribute to ARDS risk in sepsis patients as well, and we aimed to investigate the correlation of lnc‐THRIL with the risk of ARDS, dis‐ ease severity, inflammation as well as mortality in sepsis patients
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