Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Complement activation and inflammation triggered by model biomaterial surfaces

L Tang1, L Liu, H B Elwing

  • 1Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030-3498, USA.

Journal of Biomedical Materials Research
|June 25, 1998
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Nuclear transfer in sheep embryos: the effect of cell-cycle coordination between nucleus and cytoplasm and the use of in vitro matured oocytes.

Molecular reproduction and development·1997
Same author

Role of secreted proteins and gonadotrophins in promoting full maturation of porcine oocytes in vitro.

Molecular reproduction and development·1997
Same author

The responses of rat trigeminal ganglion neurons to capsaicin and two nonpungent vanilloid receptor agonists, olvanil and glyceryl nonamide.

The Journal of neuroscience : the official journal of the Society for Neuroscience·1997
Same author

Localization of human intestinal defensin 5 in Paneth cell granules.

Infection and immunity·1997
Same author

Evidence for the existence of two ATP-sensitive Rb+ occlusion pockets within the transmembrane domains of Na+/K+-ATPase.

The Journal of biological chemistry·1997
Same author

Affected members of melanoma-prone families with linkage to 9p21 but lacking mutations in CDKN2A do not harbor mutations in the coding regions of either CDKN2B or p19ARF.

Genes, chromosomes & cancer·1997
Same journal

Optimizing the tensile properties of polyvinyl alcohol hydrogel for the construction of a bioprosthetic heart valve stent.

Journal of biomedical materials research·2002
Same journal

Wear of conventional and cross-linked ultra-high-molecular-weight polyethylene acetabular cups against polished and roughened CoCr femoral heads in a biaxial hip simulator.

Journal of biomedical materials research·2002
Same journal

Immobilization of natural macromolecules on poly-L-lactic acid membrane surface in order to improve its cytocompatibility.

Journal of biomedical materials research·2002
Same journal

Light scattering and in vitro biocompatibility studies of poly (vinyl pyrrolidone) derivatives with amino-acid-dependent groups.

Journal of biomedical materials research·2002
Same journal

Immobilization of an oxalate-degrading enzyme on silicone elastomer.

Journal of biomedical materials research·2002
Same journal

An evaluation of the cytotoxic effects of orthodontic bonding adhesives upon a primary human oral gingival fibroblast culture and a permanent, human oral cancer-cell line.

Journal of biomedical materials research·2002
See all related articles

Biomaterial surfaces can trigger inflammation by activating the complement system. This study shows a direct link between complement activation on implant surfaces and the resulting inflammatory cell accumulation in vivo.

Area of Science:

  • Biomaterials Science
  • Immunology
  • Surface Chemistry

Background:

  • Biomaterial implantation often leads to inflammatory responses.
  • Complement activation by biomaterials is suspected to trigger inflammation, but direct evidence is lacking.

Purpose of the Study:

  • To establish a direct correlation between complement activation on biomaterial surfaces and subsequent inflammatory cell accumulation.
  • To investigate the influence of different surface chemistries on complement activation and inflammatory responses.

Main Methods:

  • Utilized a gold surface model with various thiol-linked functionalities.
  • Assessed in vitro complement activation (iC3b/C5b-9 generation, C3 deposition).
  • Evaluated in vivo inflammatory cell accumulation (neutrophils, monocytes/macrophages) in an animal implantation model, including complement-depleted animals.

Related Experiment Videos

Main Results:

  • Mercaptoglycerol- and mercaptoethanol-coated surfaces induced significant inflammatory cell accumulation.
  • L-cysteine, glutathione, and untreated gold surfaces showed minimal inflammatory responses.
  • Inflammatory cell accumulation on mercaptoglycerol surfaces was dependent on complement activation, as shown in complement-depleted animals.
  • A strong correlation was observed between in vitro complement activation levels and in vivo inflammatory responses.

Conclusions:

  • Surface-mediated complement activation is a key driver of inflammatory cell accumulation on biomaterial surfaces.
  • Tailoring surface chemistry can modulate complement activation and subsequent inflammatory reactions.
  • These findings provide a mechanistic link between biomaterial surface properties and host inflammatory responses.