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Accumulation of anaphylatoxins and terminal complement complexes in inflammatory fluids
A Bengtsson1, J P Bengtson, A Rydenhag
1Department of Anesthesiology and Intensive Care, Sahlgrenska Hospital, Gothenburg, Sweden.
Journal of Internal Medicine
|August 1, 1990
Summary
Complement anaphylatoxins (C3a) and terminal complement complexes (TCC) are elevated in various inflammatory fluids. These markers indicate complement activation, even with normal plasma levels, suggesting localized inflammation.
Area of Science:
- Immunology
- Biochemistry
Background:
- The complement system plays a crucial role in inflammatory responses.
- Anaphylatoxins (C3a, C5a) and terminal complement complexes (TCC) are key indicators of complement activation.
Purpose of the Study:
- To investigate the presence and concentration of C3a, C5a, and TCC in inflammatory effusions.
- To correlate fluid levels with plasma levels of these complement components.
Main Methods:
- Radioimmunoassay (RIA) was used to quantify anaphylatoxins (C3a, C5a).
- Enzyme-linked immunosorbent assay (ELISA) was employed to determine terminal complement complexes (TCC).
- Analysis was performed on inflammatory fluids (peritoneal, pleural, pericardial, burn bullae) and plasma from 33 patients.
Main Results:
- High concentrations of C3a and TCC were detected in all studied inflammatory fluids.
- Elevated C3a and TCC were observed irrespective of plasma levels, indicating localized activation.
- C5a levels were not increased in pleural or burn bullae fluid but were high in one pericarditis case and in pancreatitis with ascites.
- High TCC suggests C5a formation and subsequent removal by leukocytes in some fluids.
Conclusions:
- Complement activation, evidenced by elevated C3a and TCC, is a common feature of various inflammatory effusions.
- Local complement activation within inflammatory fluids can occur independently of systemic complement levels.
- Leukocyte interactions may influence C5a detection in inflammatory fluids.