Abstract:
:Endotoxin tolerance is an immunohomeostatic reaction to reiterant lipopolysaccharide (LPS) exposure that maintains a state of altered responsiveness in immune cells, resulting in the inhibition of the pro-inflammatory response and the resolution of inflammation. Microglia constitutes the first line of defense against endogenous and external challenges in the brain. MicroRNAs (miRs) serve a critical function in the regulation of inflammation. The aim of the present study was to investigate whether miR-155 regulates endotoxin tolerance. miR-155 and suppressor of cytokine signaling-1 (SOCS1) mRNA expression was measured using RT-qPCR. The expression of SOCS1 was measured by western blotting and immunofluorescence. TNF-α levels were detected by an enzyme-linked immunosorbent assay. The results indicated that miR-155 expression was significantly downregulated in the microglia and cortex tissue following the induction of endotoxin tolerance. This was consistent with an increase in the expression of SOCS1, a predicted target of miR-155 and key inhibitor of the inflammatory reaction. Transfection with miR-155 inhibitor significantly enhanced SOCS1 expression in the microglia following the induction of endotoxin tolerance. SOCS1 knockdown using short hairpin RNA partly inhibited the anti-inflammatory process and promoted the inflammatory response during endotoxin tolerance. The results of the current study indicate that miR-155 inhibition contributes to the development of endotoxin tolerance. Understanding how miRs regulate inflammatory mechanisms may facilitate the development of novel therapeutic strategies to treat CNS disorders.
journal_name
Exp Ther Medjournal_title
Experimental and therapeutic medicineauthors
Sun X,Sun J,Shao X,Feng J,Yan J,Qin Ydoi
10.3892/etm.2018.6032subject
Has Abstractpub_date
2018-06-01 00:00:00pages
4709-4716issue
6eissn
1792-0981issn
1792-1015pii
ETM-0-0-6032journal_volume
15pub_type
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