Blog
About

26
views
0
recommends
+1 Recommend
1 collections
    20
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      MicroRNA-21 inhibits toll-like receptor 2 agonist-induced lung inflammation in mice.

      Experimental Lung Research

      Up-Regulation, drug effects, metabolism, Female, Gene Knockdown Techniques, Humans, Immunity, Innate, Interleukin-13, pharmacology, Lipopeptides, toxicity, Mice, Mice, Inbred BALB C, MicroRNAs, antagonists & inhibitors, genetics, immunology, Pneumonia, etiology, prevention & control, Signal Transduction, Toll-Like Receptor 2, agonists, Animals, Epithelial Cells

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Impaired airway innate immunity (e.g., suppressed Toll-like receptor 2 [TLR2] signaling) has been reported in allergic lungs with bacterial infection. Recently, an allergic mouse lung milieu including the T-helper type 2 (Th2) cytokine interleukin-13 (IL-13) has been shown to up-regulate lung microRNA-21 (miR-21) expression. Whether miR-21 modulates in vivo TLR2 signaling is unknown. The goal of this study was to determine if in vivo, miR-21 regulates a TLR2 agonist-induced lung inflammatory response. Balb/c mice were intranasally pretreated with a locked nucleic acid (LNA) in vivo inhibitor probe for mouse miR-21 or a control probe, followed by intranasal instillation of a TLR2 agonist Pam3CSK4, or saline (control). Four and/or 24 hours later, mice treated with the miR-21 inhibitor probe, as compared to the control probe, significantly increased lung leukocytes, including neutrophils and the keratinocyte-derived chemokine (KC). IL-13 treatment for 72 hours increased (P < .05) miR-21 in cultured primary normal human airway epithelial cells. These results, for the first time, suggest an in vivo role of miR-21 in suppressing TLR2 signaling, and further support that IL-13 can up-regulate miR-21 in human airway epithelial cells. Functional studies on miR-21 likely provide novel approaches to modulate TLR2 signaling in Th2 cytokine-exposed airways.

          Related collections

          Author and article information

          Journal
          21892915
          10.3109/01902148.2011.596895

          Comments

          Comment on this article