Experimental Model of Pulmonary Inflammation Induced by SARS-CoV‑2 Spike Protein and Endotoxin

First published: April 7, 2022

AmbioPharm is pleased to have played a role in recently published COVID-19 research, out of the Schmidtchen Lab of Lund University, by chemically synthesizing thrombin-derived C-terminal peptide (TCP-25).  COVID-19 arises as a result of infection with the virus SARS-CoV-2 and an excessive inflammatory response can result.  The research team has published “Experimental Model of Pulmonary Inflammation Induced by SARS-CoV‑2 Spike Protein and Endotoxin” in ACS Pharmacology & Translational Science. The experimental model described could  be used for analyses of the pathophysiological features of COVID-19 and for the development of new treatments and was primarily focused on pulmonary inflammation.   

TCP-25 is a peptide that is a part of innate immunity, an inborn defense system of an organism.  TCP-25 plays a role in reducing  infection-related inflammation, and in this model, acted as a lipopolysaccharide (LPS) scavenger and CD14 blocker, both of which play a role in COVID-19 induced acute respiratory distress syndrome (ARDS).

Access the article linked here: “Experimental Model of Pulmonary Inflammation Induced by SARS-CoV‑2 Spike Protein and Endotoxin”