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.