Role of cytokines in cardiovascular diseases: a focus on endothelial responses to inflammation

Abstract

Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-alpha (tumour necrosis factor-alpha), IL (interleukin)-1, IL-6 and IFN-gamma (interferon-gamma)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-beta1 (transforming growth factor-beta1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.

The relationship between the preoperative systemic inflammatory response and cancer-specific survival in patients undergoing potentially curative resection for renal clear cell cancer

“…Firstly, that an elevated Creactive protein identifies tumours capable of producing significant amounts of proinflammatory cytokines, in particular interleukin-6 (Kinoshita et al, 1999;McKeown et al, 2004) and therefore with the potential for more rapid growth of tumour cells (Jee et al, 2001;Trikha et al, 2003). Also, that an elevated C-reactive protein identifies those patients with T-lymphocyte impairment (Maccio et al, 1998;Canna et al, 2005) or patients with a proangiogenic environment (Kofler et al, 2005;Xavier et al, 2006) allowing unrestrained tumour growth and dissemination. Clearly, both these tumour and host mechanisms may be related and required for the greater malignant potential associated with an elevated C-reactive protein concentration.…”

Molecular characterization and expression profiles in response to bacterial infection of Chinese soft-shelled turtle interleukin-8 (IL-8), the first reptilian chemokine gene

“…Other properties attributed to IL-8 include the chemoattraction of T lymphocytes [8], angiogenic activity (reviewed in Ref. [11]), stimulation of histamine release from basophils (reviewed in Ref. [12]).…”

Apolipoprotein B: a predictor of inflammatory status in postmenopausal overweight and obese women

“…Several in vitro and animal studies have demonstrated that elevated atherogenic lipoproteins lead to: (1) an increase in the adhesion of monocytes and T lymphocytes to the endothelial surface; (2) an increase in the migration of monocytes and T lymphocytes into subendothelial spaces; and (3) provision of the lipid core for the transformation of monocytes/macrophages into foam cells, which secrete several plasma inflammatory markers [8,9].…”