Platelets, small cellular fragments involved in blood clotting, are hyperactivated and dysfunctional in cystic fibrosis (CF) and crucially contribute to chronic lung inflammation, slowing down the mechanisms leading to its resolution.
Therefore, new therapeutic strategies based on platelet inhibition could help attenuate excessive lung inflammation and benefit people with CF.

In this project, the ability of certain molecules, called resolvins, to decrease excessive platelet activation was tested. 
First, with in vitro experiments on platelets and other immune system cells purified from the blood of people with CF, the researchers looked for the best resolvins capable of reducing platelet activation in the presence of different inflammatory stimuli, including Pseudomonas aeruginosa infection. In this experiment, resolvin D3 and resolvin E1 showed anti-platelet potential.
Next, resolvin D3 was tested in vivo in animal models of lung infection with CF to assess its anti-platelet potential and to determine its ability to reduce inflammation in the lungs. 

The reduced platelet activation caused by resolvin D3 was found to be associated with a lower bacterial load, less neutrophil infiltration and an overall improvement in the chronic inflammatory response in the airways.

Researchers are pursuing two lines of research based on these findings: the first one aims to characterise the biological mechanism of increased platelet activation and the consequences of its inhibition; the second one aims to search for molecules with broader pharmacological activity as a possible therapeutic development.