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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation

Published on: July 6, 2019

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MiR-155 expressed in bone marrow-derived lymphocytes promoted lipopolysaccharide-induced acute lung injury through

Yumeng Yan1, Yan Lou2, Juan Kong1

  • 1Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang, 110004, China.

Biochemical and Biophysical Research Communications
|February 6, 2019
PubMed

Insights

MicroRNA-155 (miR-155) promotes acute lung injury (ALI) by increasing inflammation. Inhibiting miR-155 in bone marrow-derived cells reduces ALI severity, suggesting a therapeutic target for this condition.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pulmonary Medicine

Background:

  • Acute lung injury (ALI) is a critical inflammatory lung condition with high mortality.
  • MicroRNA-155 (miR-155) is implicated in regulating inflammatory responses.

Purpose of the Study:

  • To investigate the specific role of miR-155 in lipopolysaccharide (LPS)-induced ALI.
  • To determine the cellular origin of miR-155 that contributes to ALI pathogenesis.

Main Methods:

  • Utilized a mouse model of LPS-induced ALI with bone marrow transplantation between miR-155 knockout and wild-type mice.
  • Assessed ALI severity by measuring pulmonary vascular leakage, edema, and neutrophil infiltration.
  • Quantified the expression of Ang-2, caspases-3 and -9, and MLC phosphorylation in lung tissues.

Main Results:

  • miR-155 knockout mice exhibited significantly reduced ALI severity following LPS injection compared to wild-type mice.
  • Key indicators of lung injury, including vascular leakage, edema, and neutrophil infiltration, were decreased in miR-155 deficient mice.
  • Bone marrow transplantation experiments revealed that miR-155 expression in bone marrow-derived lymphocytes, not lung parenchymal cells, drives inflammation.

Conclusions:

  • miR-155, particularly when expressed in bone marrow-derived lymphocytes, plays a crucial role in promoting LPS-induced ALI.
  • The pro-inflammatory effects of miR-155 in ALI are mediated through the Ang-2-Tie-2 signaling pathway.
  • Targeting miR-155 in immune cells presents a potential therapeutic strategy for managing acute lung injury.
Keywords:
Acute lung injuryAng2-Tie2 pathwayBone marrow transplantationmiR-155

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