Abstract
Hemostasis requires conversion of fibrinogen to fibrin fibers that generate a characteristic network, interact with blood cells, and initiate tissue repair. The fibrin network is porous and highly permeable, but the spatial arrangement of the external clot face is unknown. Here we show that fibrin transitioned to the blood-air interface through Langmuir film formation, producing a protective film confining clots in human and mouse models. We demonstrated that only fibrin is required for formation of the film, and that it occurred in vitro and in vivo. The fibrin film connected to the underlying clot network through tethering fibers. It was digested by plasmin, and formation of the film was prevented with surfactants. Functionally, the film retained blood cells and protected against penetration by bacterial pathogens in a murine model of dermal infection. Our data show a remarkable aspect of blood clotting in which fibrin forms a protective film covering the external surface of the clot, defending the organism against microbial invasion.
Highlights
Hemostasis is a pivotal mechanism to prevent life-threatening blood loss from sites of injury, and involves close interplay between coagulation and platelets
We show that fibrin transitioned to the blood-air interface through Langmuir film formation, producing a protective film confining clots in human and mouse models
Our data show a remarkable aspect of blood clotting in which fibrin forms a protective film covering the external surface of the clot, defending the organism against microbial invasion
Summary
Hemostasis is a pivotal mechanism to prevent life-threatening blood loss from sites of injury, and involves close interplay between coagulation and platelets. We investigated the structural characteristics of the exterior face of the blood clot and found that fibrin at the blood-air interface is not arranged in the form of fibers, but instead transitions to a continuous sheet that covers the clot surface. This sheet arises through Langmuir film formation, provides a natural limit to clot growth, prevents blood cell loss, and protects from bacterial infection. These data reveal a critical role for fibrin in hemostasis through the generation of a previously unrecognized bioprotective film that encapsulates the clot in the early stages of tissue repair
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
