Open AccessAngiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19
Author(s) -
Noof Aloufi,
Hussein Traboulsi,
Jun Ding,
Gregory Fonseca,
Parameswaran Nair,
Steven K. Huang,
Sabah N. A. Hussain,
David H. Eidelman,
Carolyn J. Baglole
Publication year - 2021
Publication title -
american journal of physiology. lung cellular and molecular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.892
H-Index - 163
eISSN - 1522-1504
pISSN - 1040-0605
DOI - 10.1152/ajplung.00455.2020
Subject(s) - copd , idiopathic pulmonary fibrosis , angiotensin converting enzyme 2 , medicine , ards , pulmonary fibrosis , pneumonia , context (archaeology) , lung , fibrosis , immunology , angiotensin ii , covid-19 , receptor , disease , biology , infectious disease (medical specialty) , paleontology
The COVID-19 pandemic is associated with severe pneumonia and acute respiratory distress syndrome leading to death in susceptible individuals. For those who recover, post-COVID-19 complications may include development of pulmonary fibrosis. Factors contributing to disease severity or development of complications are not known. Using computational analysis with experimental data, we report that idiopathic pulmonary fibrosis (IPF)- and chronic obstructive pulmonary disease (COPD)-derived lung fibroblasts express higher levels of angiotensin-converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 entry and part of the renin-angiotensin system that is antifibrotic and anti-inflammatory. In preclinical models, we found that chronic exposure to cigarette smoke, a risk factor for both COPD and IPF and potentially for SARS-CoV-2 infection, significantly increased pulmonary ACE2 protein expression. Further studies are needed to understand the functional implications of ACE2 on lung fibroblasts, a cell type that thus far has received relatively little attention in the context of COVID-19.