# Novel Link Between Myeloid-Specific Adenosine Deaminase 2 and CXCL10-CXCR3 Axis in Infectious ARDS

## TL;DR

This study finds a new connection between the enzyme ADA2 and the CXCL10-CXCR3 pathway in severe lung disease caused by SARS-CoV-2.

## Contribution

The novel link between ADA2 and the CXCL10-CXCR3 axis in infectious ARDS is identified using spatial transcriptomics and single-cell RNAseq data.

## Key findings

- ADA2 is highly expressed by inflammatory CD14+CD16+ monocytes in lungs affected by COVID-19.
- ADA2 is associated with profibrotic genes and key features of ARDS pathophysiology.
- The study links ADA2 with hypoxia and CXCR3 monocyte infiltration in ARDS.

## Abstract

Acute respiratory distress syndrome (ARDS) is a severe complication of lung injury characterized by hyperinflammation and fibrosis. Here, we show a significant association between the monocyte-derived enzyme adenosine deaminase 2 (ADA2) and SARS-CoV-2 induced ARDS. We note an interesting link between ADA2 and the chemokine CXCL10 and its receptor CXCR3. By using published datasets of spatial transcriptomics and single-cell RNAseq, we show that ADA2 is highly expressed by inflammatory CD14+CD16+ monocytes, along with profibrotic genes, in lungs affected by COVID-19. This study reveals important associations between key pathophysiological features of ARDS, linking hypoxia, infiltrative CXCR3 monocytes, and a monocyte-derived exoenzyme ADA2.