title: Expression of interleukin-32 in the inflamed arteries of patients with giant cell arteritis.
abstract: OBJECTIVE
  Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA.
  
  
  METHODS
  Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to evaluate IL-32 tissue distribution and identify IL-32-producing cells. Circulating Th1 lymphocytes were evaluated by flow cytometry.
  
  
  RESULTS
  We demonstrated a strong and significant up-regulation of IL-32 at both the messenger RNA and protein levels in the artery biopsy samples from patients with GCA. IL-32 was abundantly expressed by vascular smooth muscle cells of inflamed arteries and neovessels within inflammatory infiltrates. IL-32 expression strongly correlated with the intensity of the systemic inflammatory response. IL-32 overexpression was accompanied by strong overexpression of Th1 cytokines, such as IFNγ and IL-27p28, in inflamed arteries from GCA patients. The Th1 lymphocyte population was also expanded among peripheral blood mononuclear cells from GCA patients and produced higher amounts of IL-32 compared to controls.
  
  
  CONCLUSIONS
  Our findings indicate that overexpression of IL-32 together with a clear Th1 response immunologically characterizes the inflammatory response in GCA. In particular, IL-32 seems to be an important mediator of artery inflammation in GCA.
authors: Università di Palermo, Palermo, Italy.
authors: Francesco
authors: F
authors: Ciccia
authors: Riccardo
authors: R
authors: Alessandro
authors: Aroldo
authors: A
authors: Rizzo
authors: Simona
authors: S
authors: Principe
authors: Francesca
authors: F
authors: Raiata
authors: Alberto
authors: A
authors: Cavazza
authors: Giuliana
authors: G
authors: Guggino
authors: Antonina
authors: A
authors: Accardo-Palumbo
authors: Luigi
authors: L
authors: Boiardi
authors: Angelo
authors: A
authors: Ferrante
authors: Alfonso
authors: A
authors: Principato
authors: Annarita
authors: A
authors: Giardina
authors: Giacomo
authors: G
authors: De Leo
authors: Carlo
authors: C
authors: Salvarani
authors: Giovanni
authors: G
authors: Triolo
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D013700:Giant Cell Arteritis / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007378:Interleukins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D018417:Th1 Cells / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: C496971:IL32 protein, human; D020381:Interleukin-17; D053583:Interleukin-1beta; D015850:Interleukin-6; D007378:Interleukins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma