Correlation of small nucleolar RNA host gene 16 with acute respiratory distress syndrome occurrence and prognosis in sepsis patients

Background Long noncoding RNA small nucleolar RNA host gene 16 (lnc-SNHG16) regulates sepsis-induced acute lung injury and inflammation, which is involved in the pathophysiology of acute respiratory distress syndrome (ARDS). The present study intended to explore the role of lnc-SNHG16 as a potential biomarker indicating ARDS risk, disease severity, inflammation, and mortality in sepsis. Methods Peripheral blood mononuclear cell (PBMC) samples were collected from 160 sepsis patients within 24 hours after admission and 30 healthy controls (HCs). Then, lnc-SNHG16 in PBMCs was detected by reverse transcription-quantitative polymerase chain reaction. Sepsis patients were followed up until death or up to 28 days. Results lnc-SNHG16 was declined in sepsis patients compared with HCs (p < 0.001). The incidence of ARDS was 27.5% among sepsis patients; meanwhile, sepsis patients with ARDS had higher mortality than those without ARDS (p < 0.001). Furthermore, lnc-SNHG16 was declined in sepsis patients with ARDS compared to those without ARDS (p < 0.001); besides, higher lnc-SNHG16 was independently correlated with declined ARDS occurrence in sepsis patients (p = 0.001), while primary respiratory infection and higher CRP were independently correlated with elevated ARDS occurrence in sepsis patients (both p < 0.05). Moreover, a negative correlation was found in lnc-SNHG16 with history of diabetes, history of chronic obstructive pulmonary disease, and APACHE II and SOFA scores (all p < 0.05). Additionally, lnc-SNHG16 was declined in sepsis deaths compared with survivors (p = 0.002), while it was not independently linked with sepsis mortality. Conclusion lnc-SNHG16 correlates with lower ARDS occurrence and better prognosis in sepsis patients.