title: Role of mast cells in atherosclerosis: a classical inflammatory disease.
abstract: Atherosclerosis is an inflammatory disease and hyperlipidaemia is one of the main risk factors for aging, hypertension and diabetes. Variance in plasma LDL cholesterol concentration may be associated with differences in cardiovascular disease risk and high levels of lipids are associated with increased risk of developing atherosclerosis. Macrophages, which generate pro-inflammatory cytokines, mainly interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-alpha), are deeply involved in atherosclerosis, as well as mast cells which generate several cytokines, including IL-6 and IFN-gamma, and chemokines such as eotaxin, MCP-1 and RANTES involved in monocyte recruitment and differentiation in the arterial wall. In addition, mast cells participate in lipid retention and vascular cell remodeling, and are mediators of innate and adaptive immunity during atherosclerosis. Mast cells which accumulate in the human arterial intima and adventitia during atherosclerotic plaque progression, release vasoactive and angiogenic compounds, and pro-inflammatory mediators, such as arachidonic acid metabolites, histamine, cytokines/chemokines, platelet activating factor (PAF) and proteolytic enzymes. Mast cells can be activated by pro-inflammatory stimuli, including cytokines, hypercholesterolemia, and hyperglycemia, and trigger the endothelial expression of adhesion molecules such as P-selection, vascular cell adhesion molecule-1 (VCAM-1) and chemokines which mediate the recruitment and adhesion of leukocytes. The participation of mast cells in atherosclerosis is still an enigma and it may be of therapeutic interest to clarify this process.
authors.affiliation: Department of Surgery and Odontostomatological Sciences, University of Cagliari, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Spinas
authors.affiliation: Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.
authors.forename: S K
authors.initials: SK
authors.lastname: Kritas
authors.affiliation: Department of Dermatology, University of Rome Tor Vergata, Rome, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Saggini
authors.affiliation: Cardiology Division, Post-graduate Medical School, University of Chieti-Pescara, Chieti, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Mobili
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Caraffa
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Antinolfi
authors.affiliation: Orthopedic Division, University of Chieti-Pescara, Chieti, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Pantalone
authors.affiliation: Nicolas Foundation, Onlus, Arezzo, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Tei
authors.affiliation: Nicolas Foundation, Onlus, Arezzo, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Speziali
authors.affiliation: Department of Neurosciences and Imaging, Faculty of Medicine and Surgery, G. dAnnunzio University Chieti-Pescara, Chieti, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Saggini
authors.affiliation: Immunology Division, Post-graduate Medical School, University of Chieti-Pescara, Chieti, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Conti
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000209:etiology*; D006801:Humans; D008407:Mast Cells / Q000502:physiology*