Circulating exosomes induced by respiratory viral infections in lung transplant recipients activate cellular stress, innate immune pathways and epithelial to mesenchymal transition

Sandhya Bansal, Ajit P. Limaye, John Lee, Timothy Fleming, Christin Poulson, Ashraf Omar, Ramsey Hachem, Ankit Bharat, Ross M. Bremner, Michael A. Smith, T. Mohanakumar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Background: Chronic lung transplant rejection occurs in over 50% of lung transplant recipients and mechanism of chronic rejection is unknown. Evaluation of potential mechanism of exosomes from lung transplant recipients diagnosed with respiratory viral infection (RVI) in inducing chronic lung allograft dysfunction (CLAD). Method: Exosomes were isolated from lung transplant recipients followed by DNA and RNA isolation from exosomes. Cell signaling mechanisms were studied by co-culturing exosomes with human epithelial cells. Mice were immunized with exosomes and lung homogenates were studied for immune signaling proteins. Results: Exosomes from lung transplant recipients with RVI carry nucleic acids which are capable of inducing innate immune signaling, endoplasmic reticulum stress, and epithelial mesenchymal transition. Conclusion: Therefore, we propose that RVI can lead to induction of exosomes that initiate the process leading to CLAD in mice models. These novel findings identified the molecular mechanisms by which RVI increases the risk of CLAD.

Original languageEnglish (US)
Article number101480
JournalTransplant Immunology
Volume69
DOIs
StatePublished - Dec 2021

Keywords

  • Cell signaling
  • Exosomes
  • Lung transplant
  • Respiratory viral infection

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Transplantation

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