Abstract
Novel evidence shows that targeting the extracellular matrix remodelling and hyaluronic acid (HA) turnover have the potential to make a significant impact on the treatment of Acute Respiratory Distress Syndrome (ARDS). In this context, this project aims to elucidate the involvement of HA turnover in the development of ARDS. For this purpose, a novel in vitro ARDS model using type II human alveolar epithelial (ATII) cells stimulated with TGF-β was developed. Cell culture lysates and supernatant were collected, and HA content and molecular weight were determined. Lysates were probed for the upregulation of HA metabolic proteins by the use of PCR-RT. Immunofluorescent cell sorting was also used for the analysis of the expression of hyaluronidase (HYAL) and hyaluronic acid synthase (HAS) in the cell population of the in vitro ARDS model. Finally, two therapeutic mechanisms of action were studied in order to decrease the pro-inflammatory microenvironment observed in the ARDS model. The first mechanism suppressed HA degradation using hyaluromycin (HYAL inhibitor) and the second mechanism supressed HA biosynthesis using 4- methylumbelliferone (HAS inhibitor). For this reason, this study on the involvement of HA turnover in a ARDS model has the potential to make a significant impact on the treatment of ARDS and promote a better patient recovery and disease prognosis.
Footnotes
Cite this article as Eur Respir J 2022; 60: Suppl. 66, 2253.
This article was presented at the 2022 ERS International Congress, in session “-”.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2022
