title: Inflammatory cell phenotypes in AAAs: their role and potential as targets for therapy.
abstract: Abdominal aortic aneurysms (AAAs) are characterized by chronic inflammatory cell infiltration. AAA is typically an asymptomatic disease and caused ≈15 000 deaths annually in the United States. Previous studies have examined both human and murine aortic tissue for the presence of various inflammatory cell types. Studies show that in both human and experimental AAAs, prominent inflammatory cell infiltration, such as CD4(+) T cells and macrophages, occurs in the damaged aortic wall. These cells have the ability to undergo phenotypic modulation based on microenvironmental cues, potentially influencing disease progression. Proinflammatory CD4(+) T cells and classically activated macrophages dominate the landscape of aortic infiltrates. The skew to proinflammatory phenotypes alters disease progression and plays a role in causing chronic inflammation. The local cytokine production and presence of inflammatory mediators, such as extracellular matrix breakdown products, influence the uneven balance of the inflammatory infiltrate phenotypes. Understanding and developing new strategies that target the proinflammatory phenotype could provide useful therapeutic targets for a disease with no current pharmacological intervention.
authors.affiliation: From the Department of Pathology and Microbiology (M.A.D.) and Department of Surgery, University of Nebraska Medical Center, Omaha (M.A.D., M.K.R., B.T.B.).
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Dale
authors.affiliation: From the Department of Pathology and Microbiology (M.A.D.) and Department of Surgery, University of Nebraska Medical Center, Omaha (M.A.D., M.K.R., B.T.B.).
authors.forename: Melissa K
authors.initials: MK
authors.lastname: Ruhlman
authors.affiliation: From the Department of Pathology and Microbiology (M.A.D.) and Department of Surgery, University of Nebraska Medical Center, Omaha (M.A.D., M.K.R., B.T.B.).
authors.forename: B Timothy
authors.initials: BT
authors.lastname: Baxter
mesh_terms: D056704:Adaptive Immunity / Q000187:drug effects; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001012:Aorta, Abdominal / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D017544:Aortic Aneurysm, Abdominal / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D008407:Mast Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D058990:Molecular Targeted Therapy; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D010641:Phenotype; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators
keywords: aneurysm; aorta; inflammation; lymphocytes; macrophages