Mast cells mediate acute inflammatory responses to implanted biomaterials

摘要: Implanted biomaterials trigger acute and chronic inflammatory responses. The mechanisms involved in such responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, adhesion to implant surfaces. We earlier observed that two chemokines-macrophage protein 1alpha/monocyte chemoattractant 1-and the integrin Mac-1 (CD11b/CD18)/surface fibrinogen interaction are, respectively, required for chemotaxis adherence biomaterial However, it is still not clear how initial transmigration of phagocytes through endothelial barrier area triggered. Because implanted elicit histaminic surrounding tissue, histamine release known promote rapid diapedesis cells, we evaluated possible role mast cells recruitment implants. Using i.p. s. c. implantation polyethylene terephthalate disks mice find: (i) Extensive degranulation accompanied by release, occurs adjacent short-term (ii) Simultaneous administration H1 H2 receptor antagonists (pyrilamine famotidine, respectively) greatly diminishes both neutrophils (<20% control) monocytes/macrophages (<30% (iii) Congenitally cell-deficient also exhibit markedly reduced accumulation on s.c (iv) Finally, cell reconstitution restores "normal" conclude their granular products, especially histamine, are important Improved knowledge may permit purposeful modulation inflammation affecting biomaterials.