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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
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ORMDL3 regulates poly I:C induced inflammatory responses in airway epithelial cells.

Gemma Laura1, Yi Liu1, Kieran Fernandes1

  • 1National Heart and Lung Institute, Imperial College London, London, SW3 6LY, UK.

BMC Pulmonary Medicine
|May 18, 2021
PubMed
Summary

Orosmucoid 3 (ORMDL3) regulates airway epithelial cell inflammatory responses to viral infections. ORMDL3 deficiency reduces IL-6 and IL-8 production following poly I:C or rhinovirus stimulation, independent of TLR3 signaling.

Keywords:
Epithelial cellInflammatory responseORMDL3Poly I:CTLR3

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Area of Science:

  • Immunology
  • Respiratory Medicine
  • Cell Biology

Background:

  • Orosmucoid 3 (ORMDL3) is associated with childhood asthma and viral respiratory infections.
  • Polyinosinic-polycytidylic acid (poly I:C) mimics viral double-stranded RNA and activates Toll-like receptor 3 (TLR3).

Purpose of the Study:

  • To investigate the role of ORMDL3 in the inflammatory response of airway epithelial cells induced by poly I:C.
  • To determine if ORMDL3 influences inflammatory cytokine production during viral infections.

Main Methods:

  • Established ORMDL3 knockdown and over-expression models in human A549 and primary normal human bronchial epithelial (NHBE) cells.
  • Stimulated cells with poly I:C or IL-17A, and measured IL-6 and IL-8 levels.
  • Infected ORMDL3-deficient cells with human rhinovirus (HRV16) and assessed inflammatory markers.

Main Results:

  • ORMDL3 modulation minimally affected TLR3 transcript levels.
  • ORMDL3 deficiency attenuated IL-6 and IL-8 responses to poly I:C and HRV16.
  • ORMDL3 over-expression increased IL-6 and IL-8 release after poly I:C stimulation.

Conclusions:

  • ORMDL3 plays a regulatory role in the viral inflammatory response in airway epithelial cells.
  • This regulation occurs through mechanisms independent of the TLR3 pathway.