Abstract
BackgroundEmerging evidence shows that long noncoding RNA (lncRNA) has been a novel insight in various diseases, including pneumonia. Even though lncRNA X-inactive-specific transcript (XIST) is well studied, its role in pneumonia remains to be largely unrevealed.MethodsExpression of XIST, miRNA-30b-5p (miR-30b-5p), and CC chemokine ligand 16 (CCL16) was detected using reverse transcriptase quantitative polymerase chain reaction and western blotting; their interaction was confirmed by dual-luciferase reporter assay. Apoptosis, inflammation, and toll-like receptor 4 (TLR4)/NF-κB signaling pathway were measured using methyl thiazolyl tetrazolium assay, flow cytometry, western blotting, and enzyme-linked immunosorbent assay.ResultsLipopolysaccharide (LPS) stimulation decreased cell viability and B cell lymphoma (Bcl)-2 expression, and increased cell apoptosis rate and expression of Bcl-2-associated X protein (Bax), cleaved-caspase-3, interleukin (IL)-6, IL-1β, and tumor necrosis factor α (TNF-α) in WI-38 cells. Expression of XIST and CCL16 was upregulated in the serum of patients with pneumonia and LPS-induced WI-38 cells, respectively; silencing XIST and CCL16 could suppress LPS-induced apoptosis and inflammation in WI-38 cells, and this protection was abolished by miR-30b-5p downregulation. Moreover, XIST and CCL16 could physically bind to miR-30b-5p, and XIST regulated CCL16 expression via sponging miR-30b-5p. TLR4 and phosphorylated P65 (p-P65) and p-IκB-α were highly induced by LPS treatment, and this upregulation was diminished by blocking XIST, accompanied with CCL16 downregulation and miR-30b-5p upregulation.ConclusionsSilencing XIST could alleviate LPS-induced inflammatory injury in human lung fibroblast WI-38 cells through modulating miR-30b-5p/CCL16 axis and inhibiting TLR4/NF-κB signaling pathway.
Highlights
Pneumonia is a leading infectious cause of death, especially in the young and old people [1,2]
10 μg/mL of LPS treatment for 24 h was good enough to induce WI-38 cells (Figure 2b). These outcomes showed that LPS could induce cell apoptosis and inflammation in WI-38 cells, and X-inactive-specific transcript (XIST) and miR-30b-5p were abnormally expressed in patients with pneumonia and LPS-treated WI-38 cells
The connection between long noncoding RNA (lncRNA) and pneumonia remains to be uncovered in the upcoming years, several lncRNAs have been suggested in regulating LPSinduced cell models in pneumonia
Summary
Pneumonia is a leading infectious cause of death, especially in the young and old people [1,2]. Infantile pneumonia and community-acquired pneumonia are common types of pneumonia. The infection caused by pathogenic microorganisms, such as bacteria, mycoplasma, and viruses, leads to typical clinical symptoms of pneumonia including fever, cough with purulent sputum or blood, chest pain, and shortness of breath [3]. Pneumonia is an inflammatory disease in lower respiratory tracts [4]. Lipopolysaccharide (LPS) is the main bioactive component of Gram-negative bacteria pathogens [5] and can induce severe inflammatory response in lungs [6,7]. LPS-induced inflammatory injury is a popular model for studying the pathogenesis and management of pneumonia
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
