Long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression in several biological systems. The long intergenic RNA-erythroid pro-survival (lincRNA-EPS) has been shown to play a critical role in restraining inflammatory gene expression. However, the function of lincRNA-EPS during bacterial infections remains unknown. Here, we demonstrate that following infection with the intracellular bacterium , both mouse macrophages and dendritic cells lacking lincRNA-EPS exhibit an enhanced expression of proinflammatory cytokine genes, as well as an increased expression of the inducible nitric oxide synthase ( and nitric oxide (NO) production. Importantly, we found that lincRNA-EPS mice intraperitoneally infected with exhibit lower bacterial burdens in spleen and liver and produce more NO than control mice. Furthermore, lincRNA-EPS mice are less susceptible to a lethal dose of than wild type (WT) mice. Collectively these findings show that lincRNA-EPS suppresses host protective NO expression and impairs the host defense against infection.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6987077PMC
http://dx.doi.org/10.3389/fcimb.2019.00481DOI Listing

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