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Mast cells mediate complement activation after acid aspiration.

C Kyriakides1, W G Austen, Y Wang

  • 1Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Shock (Augusta, Ga.)
|July 10, 2001
PubMed
Summary
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Mast cells play a key role in lung injury after acid aspiration by activating the complement system. Blocking mast cell activity or substance P reduces this complement-mediated damage.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Complement System

Background:

  • Acid aspiration triggers lung injury, with the alternative complement pathway implicated.
  • Mast cells are suspected mediators of this inflammatory response.

Purpose of the Study:

  • To investigate the role of mast cells in complement activation following acid aspiration.
  • To determine if mast cell degranulation and substance P regulate this process.

Main Methods:

  • Acid aspiration was induced in mast cell-deficient (W/Wv) and wild-type mice.
  • Lung vascular permeability was measured using 125I-albumin extravasation.
  • Serum complement activity and alveolar C3 deposition were assessed.

Main Results:

Related Experiment Videos

  • Mast cell-deficient mice showed significantly reduced lung permeability compared to controls.
  • Inhibition of mast cell chymase or substance P also decreased lung injury.
  • Complement activation, indicated by C3 deposition, was prominent in wild-type mice but absent in mast cell-deficient or treated groups.

Conclusions:

  • Mast cells, through chymase activity, mediate complement activation after acid aspiration.
  • Substance P appears to regulate mast cell activation in this context.