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Published on: March 23, 2018
APT070 inhibits complement activation during in vitro cardiopulmonary bypass
Ravi J De Silva1, Alain Vuylsteke, Sarah J Fritchley
1Papworth Hospital NHS Trust, Papworth Everard, Cambridgeshire CB3 8RE, UK. ravijdesilva@doctors.org.uk
Summary
APT070, an anti-complement agent, significantly inhibited complement and neutrophil activation during in vitro cardiopulmonary bypass (CPB). This suggests APT070 may reduce CPB-induced inflammation.
Area of Science:
- Immunology
- Biochemistry
Background:
- Complement cascade proteins are crucial in inflammation and immune response.
- Complement activation occurs during cardiopulmonary bypass (CPB), potentially causing inflammation.
- APT070 is an anti-complement agent investigated for its effects on human blood during CPB.
Purpose of the Study:
- To evaluate the in vitro effect of APT070 on human blood during CPB.
- To determine if APT070 can inhibit complement activation and neutrophil stimulation.
Main Methods:
- Human blood was collected, heparinized, and treated with either APT070 (50 microg/ml) or a vehicle control.
- Blood samples were circulated in an in vitro CPB circuit for 90 minutes.
- Complement activation markers (C3a, sC5b-9) and neutrophil stimulation (CD11b expression) were measured.
Main Results:
- APT070 significantly inhibited complement activation, evidenced by reduced C3a and sC5b-9 levels (p=0.03 and p=0.01, respectively).
- APT070 significantly reduced neutrophil stimulation, as shown by decreased CD11b expression at 90 minutes (p=0.04).
Conclusions:
- APT070 effectively inhibits both complement and neutrophil activation in vitro.
- These findings suggest APT070 holds potential for mitigating the inflammatory consequences of CPB.
