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Published on: January 28, 2020
Neutrophil activation status in stable coronary artery disease
Eva Särndahl1, Ida Bergström, Veronika Patcha Brodin
1Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. eva.sarndahl@ikm.oru.se
Insights
Neutrophils in stable coronary artery disease (CAD) patients are not primed for activation. Instead, circulating neutrophils in CAD patients exhibit an impaired activation status, contrary to expectations.
Area of Science:
- Immunology
- Cardiovascular Disease
- Atherosclerosis
Background:
- Neutrophils play a significant role in atherogenesis.
- Elevated neutrophil activation is observed in unstable angina.
- A primed neutrophil state has been suggested in stable angina.
Purpose of the Study:
- To investigate the activation status of neutrophils in patients with stable coronary artery disease (CAD) undergoing conventional drug treatment.
Main Methods:
- Compared neutrophil activation markers (CD18, CD11b) and reactive oxygen species (ROS) production in 30 stable CAD patients and 30 controls.
- Utilized flow cytometry and chemiluminescence assays.
- Stimulated neutrophils with chemoattractants (Interleukin-8, Leukotriene B4) and C3bi-opsonised yeast particles.
Main Results:
- No difference in basal neutrophil CD18 expression or high-affinity CD11b state between CAD patients and controls.
- Chemoattractants did not alter neutrophil activation markers or ROS production in CAD patients compared to controls.
- ROS production in response to yeast particles and inherent ROS capacity were significantly decreased in CAD patients.
Conclusions:
- Circulating neutrophils in stable CAD patients do not show evidence of priming.
- Neutrophils in stable CAD patients demonstrate an impaired activation status.
- Further research is needed to determine if neutrophil dysfunction is a marker, atherogenic factor, or treatment consequence.
Background:
During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to investigate the neutrophil activation status in patients with stable coronary artery disease (CAD) at conventional drug treatment.
Methodology And Principal Findings:
Thirty patients with stable CAD and 30 healthy controls were included using a paired design. The neutrophil expression of CD18 and high-affinity state of CD11b was analysed by flow cytometry before and after stimulation with chemoattractants. Also, the production of reactive oxygen species (ROS) was determined by chemiluminescence. During basal conditions, the neutrophil expression of CD18 or high-affinity state of CD11b did not differ between patients and controls. Chemoattractants (Interleukin-8 and Leukotriene B(4)) did not increase either the expression or the amount of high-affinity CD11b/CD18-integrins in CAD patients compared to controls, and had no effect on the production of ROS. On the other hand, the ROS production in response to C3bi-opsonised yeast particles and the neutrophils' inherent capacity to produce ROS were both significantly decreased in patients.
Conclusion/Significance:
We could not find any evidence that neutrophils in patients with stable CAD were primed, i.e. more prone to activation, compared to cells from healthy controls. According to our data, the circulating neutrophils in CAD patients rather showed an impaired activation status. It remains to be elucidated whether the neutrophil dysfunction in CAD is mainly a marker of chronic disease, an atherogenic factor or a consequence of the drug treatment.
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