TH1/TH2 imbalance, measured by circulating and intracytoplasmic inflammatory cytokines--immunological alterations in acute coronary syndrome and stable coronary artery disease.
To describe how peripheral immune-parameters reflect the inflammatory alterations of the atherosclerotic plaques in coronary atherosclerosis. We measured general inflammatory markers C-reactive protein (CRP) and granulocyte activity, lymphocyte subpopulations and their state of activation, evaluated circulating Th1/Th2-type cytokines, and specific intracytoplasmic cytokines. We investigated the association of immune-parameters with disease outcome and mortality. Thirty-three patients with acute coronary syndrome (ACS), 62 with stable coronary artery disease (CAD) and 58 healthy controls were studied. Peripheral blood lymphocyte subgroups were quantified by flow cytometry, soluble cytokines and autoantibodies were assessed using enzyme-linked immunosorbent assay (ELISA), while intracellular cytokine levels were measured by flow cytometry after intracellular staining. We found elevated levels of CRP and granulocyte activity in ACS versus CAD (P < 0.001, P = 0.017, respectively). Natural killer (NK) cell percentages were elevated, while percentage of T cells to the total lymphocyte count was slightly decreased in ACS compared to controls (P < 0.0001, P = 0.012, respectively). Both forms of coronary atherosclerosis showed significantly higher percentages of activated T cells than controls when stained for the activation markers HLA-DR3 and CD69(+) (ACS: P < 0.0001, P = 0.002, CAD: P < 0.0001, P = 0.018, respectively). IL-1, IL-4 and IL-10 proved significantly higher in ACS versus controls (P = 0.036, P = 0.01, P < 0.0001 respectively). Th1 to Th2 ratio shifted towards a Th1 dominance in both diseases. Both general proinflammatory markers and activated T cells signify CAD. The orchestrated proinflammatory cascade eventually leads to the development of the disease.
Szodoray
P
P
3rd Department of Internal Medicine, Division of Clinical Immunology, University of Debrecen, Móricz Zs. Str. 22, 4004 Debrecen, Hungary. peter.szodoray@gades.uib.no
Timar
O
O
Veres
K
K
Der
H
H
Szomjak
E
E
Lakos
G
G
Aleksza
M
M
Nakken
B
B
Szegedi
G
G
Soltesz
P
P
D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000378:metabolism; D002308:Cardiolipins / Q000097:blood; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000276:immunology*; D003327:Coronary Disease / Q000097:blood / Q000276:immunology* / Q000401:mortality; D016207:Cytokines / Q000097:blood*; D003593:Cytoplasm / Q000737:chemistry; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D016131:Lymphocyte Subsets / Q000276:immunology; D008297:Male; D008875:Middle Aged; D018448:Models, Immunological; D011237:Predictive Value of Tests; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
D001323:Autoantibodies; D015415:Biomarkers; D002308:Cardiolipins; D016207:Cytokines; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D002097:C-Reactive Protein