Circulating levels of proinflammatory cytokines and neutrophil-platelet aggregates in patients with coronary artery disease.
Several lines of evidence indicate that increased inflammatory activity in peripheral blood is associated with the acute coronary syndrome. Systemic inflammation in clinically stable conditions of coronary artery disease has been less studied. We examined cytokine profiles in 20 patients who had acute coronary syndrome, 45 who had angiographically verified coronary artery disease and stable angina pectoris, and 45 healthy controls. Circulating levels of C-reactive protein, interleukin-1 receptor antagonist, interleukin-2 receptor, interleukin-6, interleukin-10, and interleukin-18 were determined. Subpopulations of peripheral immune cells, including neutrophil-platelet aggregates, were analyzed by 3-color flow cytometry using a panel of monoclonal antibodies. Patients who had acute coronary syndrome and stable angina pectoris had significantly higher levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist than did controls, whereas levels of interleukin-2 receptor, interleukin-10, and interleukin-18 were similar across groups. Patients had significantly more neutrophils, and the numbers of neutrophil-platelet aggregates were particularly large in patients who had stable angina pectoris. High levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist in patients were significantly related to numbers of neutrophils and neutrophil-platelet aggregates but not to other immune cell subpopulations. The data suggest that the interaction between neutrophils and platelets is an important component of proinflammatory activity seen in peripheral blood of stable and unstable forms of coronary artery disease.
Nijm
Johnny
J
Research Center of Cardiovascular Disease, Högland Hospital, Eksjö, Sweden. jonny.nijm@lj.se
Wikby
Anders
A
Tompa
Andrea
A
Olsson
Anders G
AG
Jonasson
Lena
L
D000787:Angina Pectoris / Q000276:immunology / Q000378:metabolism; D000789:Angina, Unstable / Q000276:immunology / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis*; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007378:Interleukins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism*; D010974:Platelet Aggregation / Q000502:physiology*; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D015375:Receptors, Interleukin-2 / Q000097:blood; D011994:Recombinant Proteins / Q000097:blood; D012795:Sialoglycoproteins / Q000097:blood; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007378:Interleukins; D017472:Receptors, Interleukin-1; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D012795:Sialoglycoproteins; D014280:Triglycerides; D002097:C-Reactive Protein