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RESEARCH PRODUCT
Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis
Alfonso PrincipatoA Accardo-palumboCarlo SalvaraniFrancesca RaiataGiuliana GugginoSimona PrincipeGiacomo De LeoLuigi BoiardiAroldo RizzoFrancesco CicciaAngelo FerranteGiovanni TrioloAnnarita GiardinaAlberto CavazzaRiccardo Alessandrosubject
MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNAdescription
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. Conclusion 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2011-01-01 |