Microvascular effects of anaphylatoxins C3a and C5a.
Abstract
The direct microvascular effects of human C3a and C5a were investigated by using hamster cheek pouches prepared for intravital microscopy. Topical application of 10 nM C3a resulted in pronounced microcirculatory alterations, characterized by vasoconstriction, platelet aggregation, and an increase in macromolecular leakage at postcapillary venules, as assessed by extravasation of intravascular fluorescein-labeled dextran (m.w. 150,000). Exposure of the preparation to 500 nM COOH-terminal octapeptide analogs of C3a resulted in a microvascular response almost identical to that of C3a, supporting the view that the active site of this anaphylatoxin resided within the COOH-terminal portion. Changes similar to those caused by C3a were also induced by 20 or 100 nM C5a and, in addition, the higher concentration of C5a caused accumulation of polymorphonuclear leukocytes (PMNL) in small venules and somewhat prolonged vascular leakage from venules exhibiting PMNL accumulation. Histamine was found to partially mediate the vascular leakage induced by C3a and the initial (first 5 min) permeability response to the high concentration of C5a, whereas the subsequent leakage induced by the latter anaphylatoxin was unaffected by mepyramine pretreatment. In neutropenic and mepyramine-treated animals exposed to the high concentration of C5a, a partial reduction of both the early and the subsequent vascular leakage was seen, indicating that accumulated PMNL play a role in the prolonged phase of leakage. The pronounced microvascular alterations induced by low concentrations of C3a and C5a strengthen the view that these anaphylatoxins act as mediators of inflammatory reactions in which the complement system is activated.
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“Some of its effects include myocardial dysfunction, increased tissue oxygen demand, complement activation, contact activation, coagulopathy, and microvascular thrombosis with subsequent organ failure.(7-9) Endogenous endotoxin immunity (antibodies to various serotypes of endotoxin) is conferred early in fetal life fro…”
BackgroundEffects of systemic complement activation on renal circulation of rats
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From infection to repair: Understanding the workings of our innate immune cells
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Tear fluid and complement activation products in tears after ocular surgery
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“Degranulation of platelets then induces C3 [12], which generates C3a and C5a that cause migration, activation, and aggregation of mast cells, polymorphonuclear cells, and macrophages [23, 24], all involved in tissue clearance.”
BackgroundSialogenins and Immunomodulators Derived from Blood Feeding Parasites
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- Authors
- Björk, J., Hugli, T. E., & Smedegård, G.
- Affiliations
- Uppsala University (SE)
- Scripps Clinic (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1985-02-01
- Volume
- 134
- Issue
- 2
- Pages
- 1115-1119
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1583938359
- Cited by
- 134
- References
- 0
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 5 · 2015: 3 · 2014: 3 · 2013: 3
- FWCI
- 2.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Keywords
- anaphylatoxins, C3a, C5a, complement system, microcirculation, vasoconstriction, platelet aggregation, vascular leakage, polymorphonuclear leukocytes, histamine, mepyramine, neutropenia, inflammatory mediators, hamster cheek pouch
- MeSH terms
- Animals, Arterioles, Cheek, Complement C3, Complement C5, Cricetinae, Histamine, Humans, Male, Mesocricetus, Microcirculation, Oligopeptides, Platelet Aggregation, Pyrilamine, Vasoconstriction, Venules, Complement C3a, Complement C5a
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