Mast cells mediate acute inflammatory responses to implanted biomaterials

Abstract

Implanted biomaterials trigger acute and chronic inf lammatory responses. The mechanisms involved in such acute inf lammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokinesmacrophage inf lammatory protein 1␣͞monocyte chemoattractant protein 1-and the phagocyte integrin Mac-1 (CD11b͞CD18)͞surface fibrinogen interaction are, respectively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear

Medical biofilms

“…As leukocytes arrive at the site of injury, they, too, begin to produce various growth factors and cytokines that attract more inflammatory cells. MIP-1a and MCP-1 have been implicated in phagocyte chemotaxis towards implants (Tang et al, 1998).…”

Acute phase response in patients undergoing lumbar spinal surgery: modulation by perioperative treatment with naproxen and famotidine

“…These changes may be mediated by a direct action of famotidine on hepatic H2 receptors [14] which could regulate, at least in part, IL-6-induced APP synthesis, and by a lower hepatic IL-1 receptor expression induced by naproxen, as has been seen in synovial cells and chondrocytes [22,23]. In addition, results from experimental research suggest that granular products of mast cells, espe-371 cially histamine, are involved in both acute and chronic inflammation affecting implanted biomaterial and that simultaneous administration of histamine H1 and H2 receptor antagonists (pyralamine and famotidine, respectively), greatly diminishes histamine effects [30]. Finally, an effect of tramadol can not be completely ruled out.…”

The connective tissue response to Ti, NiCr and AgPd alloys.

“…Human MCs release tryptase, which, in concentrations of 0.3-3 nM, stimulates the synthesis of mRNA procollagen [39]. Tryptase simultaneously intensifies fibroblast migration and proliferation without influencing (intercellular) matrix metalloproteinase [40]. Mastocytes contain the heparin linked with the basic fibroblast growth factor (bFGF) in granules, and upon heparin release, they simultaneously release bFGF, which intensifies fibroblast proliferation [41].…”