Cargo-free particles divert neutrophil-platelet aggregates to reduce thromboinflammation.
Alison L BankaM Valentina GuevaraEmma R BrannonNhien Q NguyenShuang SongGillian CadyDavid J PinskyKathryn E UhrichReheman AdiliMichael A HolinstatOmolola Eniola-AdefesoPublished in: Nature communications (2023)
The combination of inflammation and thrombosis is a hallmark of many cardiovascular diseases. Under such conditions, platelets are recruited to an area of inflammation by forming platelet-leukocyte aggregates via interaction of PSGL-1 on leukocytes and P-selectin on activated platelets, which can bind to the endothelium. While particulate drug carriers have been utilized to passively redirect leukocytes from areas of inflammation, the downstream impact of these carriers on platelet accumulation in thromboinflammatory conditions has yet to be studied. Here, we explore the ability of polymeric particles to divert platelets away from inflamed blood vessels both in vitro and in vivo. We find that untargeted and targeted micron-sized polymeric particles can successfully reduce platelet adhesion to an inflamed endothelial monolayer in vitro in blood flow systems and in vivo in a lipopolysaccharide-induced, systemic inflammation murine model. Our data represent initial work in developing cargo-free, anti-platelet therapeutics specifically for conditions of thromboinflammation.
Keyphrases
- lipopolysaccharide induced
- blood flow
- oxidative stress
- drug delivery
- inflammatory response
- cardiovascular disease
- cancer therapy
- peripheral blood
- small molecule
- mass spectrometry
- emergency department
- cystic fibrosis
- drug release
- cardiovascular risk factors
- electronic health record
- endothelial cells
- coronary artery disease
- liquid chromatography
- deep learning
- tandem mass spectrometry
- machine learning