Autoregulation of thromboinflammation on biomaterial surfaces by a multicomponent therapeutic coating

• Activation of the thrombotic and complement systems is the main recognition and effector mechanisms in the multiple adverse biological responses triggered when biomaterials or therapeutic cells come into blood contact. We have created a surface which is auto-protective to human innate immunity by combining three fundamentally different strategies, all developed by us previously, which have been shown to induce substantial, but incomplete hemocompatibility when used separately. In summary, we have conjugated a factor H-binding peptide; and an ADP-degrading enzyme; using a PEG linker on both material and cellular surfaces. When exposed to human whole blood, factor H was specifically recruited to the modified surfaces and inhibited complement attack. In addition, activation of platelets and coagulation was efficiently attenuated, by degrading ADP. Thus, by inhibiting thromboinflammation using a multicomponent approach, we have created a hybrid surface with the potential to greatly reduce incompatibility reactions involving biomaterials and transplantation.

Ämnesord

NATURVETENSKAP  -- Biologi (hsv//swe)

NATURAL SCIENCES  -- Biological Sciences (hsv//eng)

Nyckelord

Apyrase

Coagulation

Complement

Factor H-binding peptide

Poly(ethylene glycol) (PEG)

Surface modification

Autoregulations

Biological response

Biomaterial surfaces

Blood contact

Complement systems

H-binding

Hemocompatibility

Hybrid surface

Innate immunity

Modified surfaces

Multicomponents

Whole blood

Biological materials

Biomaterials

Peptides

Polyethylene glycols

Surface treatment

Surfaces

5C6 peptide

biomaterial

complement factor H

macrogol

peptide

unclassified drug

article

autoregulation

biotinylation

endothelium cell

erythrocyte

human

inflammation

multicomponent therapeutic coating

peptide synthesis

porcine aortic endothelial cell

priority journal

protein immobilization

thromboinflammation

Biomedical Sciences

Publikations- och innehållstyp

ref (ämneskategori)

art (ämneskategori)