Role of Novel Biomarkers of Inflammation in Patients With Stable Coronary Heart Disease

Abstract

Atherosclerosis is a dynamic chronic inflammatory process, and some inflammatory biomarkers have roles in this process. The levels of C-reactive protein (CRP) in patients with chronic stable coronary heart disease (CHD) have not been investigated well, and the levels of macrophage colony-stimulating factor (M-CSF) and interleukin-3 (IL-3) in patients with chronic stable CHD and the effects of these cytokines on atherogenesis are not known. To determine whether new inflammatory biomarkers have roles in atherosclerosis, the authors measured the levels of CRP, M-CSF, and IL-3 in patients with chronic stable CHD and in healthy controls. They measured plasma CRP concentrations by using a highly sensitive CRP reagent with immunonephelometric method, and plasma M-CSF and IL-3 concentrations with the help of a commercial enzyme-linked immunoassay test in 31 patients with chronic stable CHD documented by coronary angiography and in 22 age-matched healthy control subjects documented by coronary angiography. Mean plasma CRP, M-CSF, and IL-3 concentrations in patients with chronic stable CHD were significantly higher than those in controls (8.2 vs 4.6 mg/L, 195.3 vs 28.9 pg/mL, 173 vs 118 ng/mL, respectively, ppi.05). CRP, M-CSF, and IL-3 were all increased in patients with chronic stable CHD relative to controls. These findings suggest that these are new inflammatory biomarkers that may have important roles in the development of atherosclerotic lesions.

Increased leptin expression selectively in the hypothalamus suppresses inflammatory markers CRP and IL-6 in leptin-deficient diabetic obese mice

“…A similar outcome of a single central injection of rAAV-lep persisting for longer periods was observed in wt rodents and ob/ ob mice [6][7][8][9]14,32,46,47]. The efficacy of the stable leptin expression, specifically in the hypothalamus in minute amounts, to curb accumulation of fat for the lifetime of rodents is important because excessive long-term secretion of several adipokines contributes to a state of chronic, systemic and local vascular inflammation as the volume of adipose tissue, especially visceral adipose tissue, expands [19,21,33,34,36,38,42,45]. The co-morbidities of obesity, in particular CVD and diabetes, are hypothesized to be due, in part, to persistence of chronic lowgrade, subclinical inflammation.…”

“…Clinical investigations have also uncovered a strong relationship between obesity and chronic low-grade inflammation [40,45]. In fact, it is generally held that chronic low-grade inflammation is a causative factor in CVD and diabetes mellitus, as well as other metabolic disorders linked to or exacerbated by obesity [36,45]. Elevations in circulating levels of acutephase proteins, such as C-reactive protein (CRP), and pro-inflammatory cytokines, such as interleukin-6 (IL-6), in obese individuals are consistent with these findings [27,36,40,45].…”

“…In fact, it is generally held that chronic low-grade inflammation is a causative factor in CVD and diabetes mellitus, as well as other metabolic disorders linked to or exacerbated by obesity [36,45]. Elevations in circulating levels of acutephase proteins, such as C-reactive protein (CRP), and pro-inflammatory cytokines, such as interleukin-6 (IL-6), in obese individuals are consistent with these findings [27,36,40,45]. CRP is a sensitive, though relatively non-specific, biomarker of systemic inflammation and has been identified as a predictor of risks for CVD [27].…”

Novel Aspects of Glucocorticoids Actions on Energy Homeostasis and Hydromineral Balance

“…In fact, inflammation may contribute to a range of metabolic disturbances related to obesity, such as diabetes mellitus and cardiovascular diseases (Oren et al, 2007). Rats fed with high-fat diet express high levels of TNF-, IL-6 and IL-1 in the hypothalamus, which is consistent with the development of an inflammatory process (Milanski et al, 2009).…”

Az ösztrogénhiány, elhízás és a szabadidős testmozgás hatásának vizsgálata állatkísérletes modellekben

“…A MPO az LDLkoleszterinhez kötődve serkenti a habos sejtek kialakulását, mely hozzájárul az atheroszklerotikus plakk-képződéshez. A MPO-katalizált oxidáció eredményeként a fiziológiai körülmények között kardioprotektív hatású HDL-koleszterin diszfunkciója is megfigyelhető [128]. Klinikai vizsgálatok igazolják, hogy a MPO enzim a mátrix metalloproteázok aktiválásával, illetve a mátrix metalloproteáz szöveti inhibítorok deaktiválásával gyengítik a plakk fibrózus sapkáját, így növelik a plakkruptúra veszélyét [129,130].…”