Sepsis is commonly complicated by
acute lung injury (ALI). We aimed to determine the long non-coding RNAs (lncRNAs) and mRNAs expression profiles. Septic
acute lung injury mouse model was established by cecal
ligation and
puncture. LPS was applied to induce
inflammation in mouse alveolar macrophages (MH-s). Besides, LPS/
Nigericin sodium salt was used to activate
inflammasome in MH-s.
LncRNA and
mRNA profiles were detected using an Agilent microarray and identified by qPCR. Bioinformatic analyses were employed to analyze the expression profiles and multiple biological functions.
Inflammation-related mRNAs were selected according to KEGG pathways and GO terms including
inflammation response, immune response and
cytokine activity. A network of
inflammation related mRNAs and co-expressed lncRNAs was conducted. Finally, Gm33647 was identified as potential regulator in septic
acute lung injury. Gm33647 was knock-downed via
siRNA to explore functions. The results showed 353 differentially expressed lncRNAs and 3116 differentially expressed mRNAs were identified. Co-expression networks of
lncRNA-
mRNA showed Gm33647 was a hub gene. Cis- and trans-regulation analyses revealed Gm41442, Gm38850 and Gm36841 could function as a network in septic ALI.
LncRNA Gm33647 was reduced by LPS and increased by
inflammasome activation in MH-s. Silencing Gm33647 up-regulated
IL-6,
IL10 and TNF-α in MH-s. When
inflammasome was activated by LPS/
Nigericin sodium salt, IL-1β,
IL-18 and
Caspase 1 were increased by silencing Gm33647 in MH-s. These results identified
inflammation related lncRNAs and Gm33647 as potential regulators in septic ALI.