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Complement C3 participation in monocyte adhesion to different surfaces

A K McNally1, J M Anderson

  • 1Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.

Proceedings of the National Academy of Sciences of the United States of America
|October 11, 1994
PubMed
Summary
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Monocyte adhesion to biomaterials involves complement component C3 and leukocyte integrins like CD11b/CD18. Fibrinogen can alter these adhesion mechanisms on different material surfaces.

Area of Science:

  • Biomaterials Science
  • Immunology
  • Cell Biology

Background:

  • Monocyte/macrophage interactions with biomaterials are crucial for biocompatibility.
  • Understanding cell adhesion mechanisms on materials is key to predicting in vivo responses.
  • The progression from monocyte to foreign body giant cell involves surface interactions.

Purpose of the Study:

  • To identify adhesion mechanisms mediating human blood monocyte adhesion to various biomaterial surfaces in vitro.
  • To investigate the role of complement component C3 and leukocyte integrins in monocyte adhesion.
  • To explore how surface properties influence the adsorption of adhesion-mediating proteins.

Main Methods:

  • Utilized modified polystyrenes with different surface chemistries (fluorinated, siliconized, nitrogenated, oxygenated).

Related Experiment Videos

  • Employed complement component C3-depleted serum and replenished with purified C3.
  • Used monoclonal antibodies (mAbs) targeting leukocyte integrin subunits CD18 and CD11b.

    • Main Results:

    • Monocyte adhesion decreased significantly (50-100%) with C3-depleted serum, varying by surface.
    • Adhesion was restored upon replenishment of C3, indicating its importance.
    • Monoclonal antibodies against CD18 and CD11b inhibited adhesion, suggesting C3bi-integrin interactions.
    • Adsorbed fibrinogen reduced the efficacy of these antibodies, pointing to alternative adhesion pathways.

    Conclusions:

    • Complement component C3 plays a significant role in monocyte adhesion to diverse biomaterial surfaces.
    • The leukocyte integrin CD11b/CD18 mediates adhesion, likely through interactions with adsorbed C3bi.
    • Fibrinogen adsorption can modulate or override C3bi-integrin mediated adhesion, highlighting surface-dependent mechanisms.