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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
Insights
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.
Background:
The proteins of the complement cascade play an important role in inflammation and the immune response. They have been shown to be activated during cardiopulmonary bypass (CPB), and may be responsible for the inflammatory response to CPB. We looked at the effect of APT070, an anti-complement agent, on human blood during in vitro CPB.
Materials And Methods:
Four hundred millilitres of blood was venesected from healthy human volunteers and heparinised. To the blood was added either APT070 to a concentration of 50 microg/ml (n=5) or vehicle control (n=4). The blood was entered into an in vitro CPB circuit and circulated for 90 min.
Results:
Our results showed that after 90 min of in vitro bypass APT070 significantly inhibited the activation of compliment as demonstrated by C3a (p=0.03) and sC5b-9 (p=0.01) levels, and reduced neutrophil stimulation as measured by CD11b expression (p=0.04 at 90 min).
Conclusion:
APT070 significantly inhibits complement and neutrophil activation. This result may have considerable implications, especially if it can be shown to decrease the inflammatory sequelae of CPB.
