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Inflammation and Atherosclerosis pp 197–217Cite as

Mediators of Vascular Inflammation

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Abstract

Inflammation is a basic pathological mechanism that underlies a variety of diseases. The inflammatory reaction involves the complex interactions between inflammatory cells (neutrophils, lymphocytes and monocytes/macrophages) and vascular cells (endothelial [EC] and smooth muscle cells [SMC]). The role of vascular cells during the inflammatory process is critical. Multiple cytokines and growth factors are present at sites of inflammation, and each of these can potentially influence the nature of the inflammatory response [1]. EC and SMC must integrate the signals generated by these multiple factors to effectively regulate the immuno-inflammatory response through the expression of adhesion molecules, cytokines, chemokines, matrix metalloproteinases (MMPs) and growth factors. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli, as well as in the identification of the major intracellular inflammatory signaling pathways, NF-κB, AP-1 and JAK/STAT. Much recent works show that vascular inflammation can be limited by anti-inflammatory counter regulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. This might be of particular importance in inflammatory diseases such as atherosclerosis, aneurysm, septic shock or ischemia/reperfusion. Critically situated at the boundary between blood and tissues, the endothelium is a focus for inflammatory processes. EC receive signals from humoral factors, inflammatory mediators, and physical forces from both the circulation and the tissue. A number of potential triggers capable of inducing proinflammatory and prothrombotic cellular responses have been identified; these include modified lipoproteins, proinflammatory cytokines, chemokines, vasoactive peptides (angiotensin II, endothelin), neuropeptides (substance P), hyperglycemia and advanced glycosylated end products (AGE), smoking, oxidative stress [2]. SMC also are targets of these triggers. The purpose of the present review is to describe recent advances in the understanding of the mechanisms of vascular inflammation.

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Authors and Affiliations

  1. Paris-Cardiovascular Research center (PARCC), INSERM U970, 56 rue Leblanc, 75015, Paris, France

    Hafid Ait-Oufella, Ziad Mallat & Alain Tedgui

  2. University Paris Descartes, Paris, France

    Hafid Ait-Oufella, Ziad Mallat & Alain Tedgui

Authors
  1. Hafid Ait-Oufella
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  2. Ziad Mallat
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  3. Alain Tedgui
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Corresponding author

Correspondence to Alain Tedgui .

Editor information

Editors and Affiliations

  1. Medical University Innsbruck, Peter-Mayr-Strasse 4 a, Innsbruck, 6020, Austria

    Georg Wick

  2. Laboratory of Autoimmunity, Division of Experimental Pathophysiology, Biocenter, Innsbruck Medical University, Schöpfstraße 41, Innsbruck, 6020, Austria

    Cecilia Grundtman

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© 2012 Springer-Verlag/Wien

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Ait-Oufella, H., Mallat, Z., Tedgui, A. (2012). Mediators of Vascular Inflammation. In: Wick, G., Grundtman, C. (eds) Inflammation and Atherosclerosis. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0338-8_10

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