Immune complexes mediate rapid alterations in microvascular permeability: roles for neutrophils, complement, and
Karyn J Lister1, Will G James, Michael J Hickey
1Centre for Inflammatory Diseases, Monash University, Victoria, Australia.
Microcirculation (New York, N.Y. : 1994)
|September 22, 2007
Summary
Immune complexes rapidly increase microvascular permeability and leukocyte recruitment, involving complement and neutrophils. Platelets play a key role in this immune response.
Area of Science:
- Immunology
- Microvascular Biology
- Inflammation Research
Background:
- Immune complex-induced responses involve complex cellular and molecular interactions.
- The precise mechanisms initiating these responses, particularly in the microvasculature, require further elucidation.
Purpose of the Study:
- To investigate the immediate microvascular response following immune complex formation.
- To understand the interplay of cellular and molecular pathways in the early stages of immune complex-induced inflammation.
Main Methods:
- Utilized the reverse passive Arthus (RPA) model in mouse cremaster muscle.
- Employed intravital microscopy to assess microvascular permeability (FITC-dextran leakage) and leukocyte-endothelial interactions.
- Investigated the roles of platelet-activating factor (PAF), leukotrienes, complement component C3, and platelets through inhibition and depletion studies.
Main Results:
- Immune complex deposition triggered rapid increases in microvascular permeability and leukocyte adhesion/emigration.
- Inhibition of PAF and leukotrienes, C3 depletion, and leukocyte adhesion blockade all reduced permeability and leukocyte recruitment.
- Mast cell stabilization modulated leukocyte behavior but accelerated permeability increases, while platelet depletion delayed permeability changes and inhibited leukocyte recruitment.
Conclusions:
- Immune complexes induce rapid, complement-dependent leukocyte recruitment and neutrophil-dependent microvascular dysfunction.
- Platelets are identified as crucial mediators promoting leukocyte recruitment in immune complex-induced inflammation.
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