Decreased plasma cartilage acidic protein 1 in COVID‐19

Author:

Johansson Mats W.123ORCID,Balnis Joseph45,Muehlbauer Laura K.67,Bukhman Yury V.1,Stefely Matthew S.1,Overmyer Katherine A.16,Vancavage Rachel45,Tiwari Anupama45,Adhikari Anish Raj45,Feustel Paul J.8,Schwartz Bradford S.123,Coon Joshua J.1267,Stewart Ron1,Jaitovich Ariel45,Mosher Deane F.123

Affiliation:

1. Morgridge Institute for Research Madison Wisconsin USA

2. Department of Biomolecular Chemistry University of Wisconsin‐Madison Madison Wisconsin USA

3. Department of Medicine University of Wisconsin‐Madison Madison Wisconsin USA

4. Division of Pulmonary and Critical Care Medicine Albany Medical Center Albany New York USA

5. Department of Molecular and Cellular Physiology Albany Medical College Albany New York USA

6. National Center for Quantitative Biology of Complex Systems Madison Wisconsin USA

7. Department of Chemistry University of Wisconsin‐Madison Madison Wisconsin USA

8. Department of Neuroscience and Experimental Therapeutics Albany Medical College Albany New York USA

Abstract

AbstractCartilage acidic protein‐1 (CRTAC1) is produced by several cell types, including Type 2 alveolar epithelial (T2AE) cells that are targeted by SARS‐CoV2. Plasma CRTAC1 is known based on proteomic surveys to be low in patients with severe COVID‐19. Using an ELISA, we found that patients treated for COVID‐19 in an ICU almost uniformly had plasma concentrations of CRTAC1 below those of healthy controls. Magnitude of decrease in CRTAC1 distinguished COVID‐19 from other causes of acute respiratory decompensation and correlated with established metrics of COVID‐19 severity. CRTAC1 concentrations below those of controls were found in some patients a year after hospitalization with COVID‐19, long COVID after less severe COVID‐19, or chronic obstructive pulmonary disease. Decreases in CRTAC1 in severe COVID‐19 correlated (r = 0.37, p = 0.0001) with decreases in CFP (properdin), which interacts with CRTAC1. Thus, decreases of CRTAC1 associated with severe COVID‐19 may result from loss of production by T2AE cells or co‐depletion with CFP. Determination of significance of and reasons behind decreased CRTAC1 concentration in a subset of patients with long COVID will require analysis of roles of preexisting lung disease, impact of prior acute COVID‐19, age, and other confounding variables in a larger number of patients.

Funder

National Institutes of Health

Publisher

Wiley

Subject

Physiology (medical),Physiology

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