IL-33 is overexpressed in the inflamed arteries of patients with giant cell arteritis

Francesco Ciccia, Riccardo Alessandro, Aroldo Rizzo, Stefania Raimondo, AnnaRita Giardina, Francesca Raiata, Luigi Boiardi, Alberto Cavazza, Giuliana Guggino, Giacomo De Leo, Carlo Salvarani, Giovanni Triolo

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Abstract

Objective: To study the expression of interleukin (IL)-33 and to evaluate its relationship with macrophage polarisation in artery biopsy specimens from patients with giant cell arteritis (GCA). Methods: IL-33, ST2, p-STAT-6 and perivascular IL-1 receptor-associated kinase 1 (p-IRAK1) tissue distribution was evaluated by immunohistochemistry. Inducible nitric oxide synthase and CD163 were also used by immunohistochemistry to evaluate the M1 and M2 polarisation, respectively. Quantitative gene expression analysis of IL-33, T-helper (Th)2-related transcription factor STAT6, Th2 cytokines (IL-4, IL-5, IL-25) and interferon (IFN)-γ was performed in artery biopsy samples obtained from 20 patients with GCA and 15 controls. Five additional patients who had received prednisone when the temporal artery biopsy was performed were also enrolled. Results: IFN-γ and IL-33 were significantly overexpressed in the in flamed arteries of GCA patients. IL-33 overexpression was not accompanied by a concomitant increase of Th2 cytokines. Neovessels scattered through the inflammatory infiltrates were the main sites of IL-33 expression. The expression of IL-33 receptor ST2 and of p-IRAK1 was also increased in GCA patients. Arteries from glucocorticoid-treated patients had a lower expression of IL-33. IL-33 was accompanied by the expression of p-STAT6 and a clear M2 macrophages polarisation. Conclusions: A role for IL-33 in the inflammation of GCA patients is supported by these findings.

Original languageEnglish
Pages (from-to)258-264
Number of pages7
JournalAnnals of the Rheumatic Diseases
Volume72
Issue number2
DOIs
Publication statusPublished - Feb 2013

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Giant Cell Arteritis
Arteries
Biopsy
Interleukin-1 Receptor-Associated Kinases
Macrophages
Polarization
Interferons
STAT6 Transcription Factor
Immunohistochemistry
Cytokines
Interleukin-33
Temporal Arteries
Interleukin-17
Interleukin-5
Nitric Oxide Synthase Type II
Tissue Distribution
Prednisone
Interleukin-4
Glucocorticoids
Gene expression

ASJC Scopus subject areas

  • Rheumatology
  • Immunology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Allergy

Cite this

Ciccia, F., Alessandro, R., Rizzo, A., Raimondo, S., Giardina, A., Raiata, F., ... Triolo, G. (2013). IL-33 is overexpressed in the inflamed arteries of patients with giant cell arteritis. Annals of the Rheumatic Diseases, 72(2), 258-264. https://doi.org/10.1136/annrheumdis-2012-201309

IL-33 is overexpressed in the inflamed arteries of patients with giant cell arteritis. / Ciccia, Francesco; Alessandro, Riccardo; Rizzo, Aroldo; Raimondo, Stefania; Giardina, AnnaRita; Raiata, Francesca; Boiardi, Luigi; Cavazza, Alberto; Guggino, Giuliana; De Leo, Giacomo; Salvarani, Carlo; Triolo, Giovanni.

In: Annals of the Rheumatic Diseases, Vol. 72, No. 2, 02.2013, p. 258-264.

Research output: Contribution to journalArticle

Ciccia, F, Alessandro, R, Rizzo, A, Raimondo, S, Giardina, A, Raiata, F, Boiardi, L, Cavazza, A, Guggino, G, De Leo, G, Salvarani, C & Triolo, G 2013, 'IL-33 is overexpressed in the inflamed arteries of patients with giant cell arteritis', Annals of the Rheumatic Diseases, vol. 72, no. 2, pp. 258-264. https://doi.org/10.1136/annrheumdis-2012-201309
Ciccia, Francesco ; Alessandro, Riccardo ; Rizzo, Aroldo ; Raimondo, Stefania ; Giardina, AnnaRita ; Raiata, Francesca ; Boiardi, Luigi ; Cavazza, Alberto ; Guggino, Giuliana ; De Leo, Giacomo ; Salvarani, Carlo ; Triolo, Giovanni. / IL-33 is overexpressed in the inflamed arteries of patients with giant cell arteritis. In: Annals of the Rheumatic Diseases. 2013 ; Vol. 72, No. 2. pp. 258-264.
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abstract = "Objective: To study the expression of interleukin (IL)-33 and to evaluate its relationship with macrophage polarisation in artery biopsy specimens from patients with giant cell arteritis (GCA). Methods: IL-33, ST2, p-STAT-6 and perivascular IL-1 receptor-associated kinase 1 (p-IRAK1) tissue distribution was evaluated by immunohistochemistry. Inducible nitric oxide synthase and CD163 were also used by immunohistochemistry to evaluate the M1 and M2 polarisation, respectively. Quantitative gene expression analysis of IL-33, T-helper (Th)2-related transcription factor STAT6, Th2 cytokines (IL-4, IL-5, IL-25) and interferon (IFN)-γ was performed in artery biopsy samples obtained from 20 patients with GCA and 15 controls. Five additional patients who had received prednisone when the temporal artery biopsy was performed were also enrolled. Results: IFN-γ and IL-33 were significantly overexpressed in the in flamed arteries of GCA patients. IL-33 overexpression was not accompanied by a concomitant increase of Th2 cytokines. Neovessels scattered through the inflammatory infiltrates were the main sites of IL-33 expression. The expression of IL-33 receptor ST2 and of p-IRAK1 was also increased in GCA patients. Arteries from glucocorticoid-treated patients had a lower expression of IL-33. IL-33 was accompanied by the expression of p-STAT6 and a clear M2 macrophages polarisation. Conclusions: A role for IL-33 in the inflammation of GCA patients is supported by these findings.",
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AU - Ciccia, Francesco

AU - Alessandro, Riccardo

AU - Rizzo, Aroldo

AU - Raimondo, Stefania

AU - Giardina, AnnaRita

AU - Raiata, Francesca

AU - Boiardi, Luigi

AU - Cavazza, Alberto

AU - Guggino, Giuliana

AU - De Leo, Giacomo

AU - Salvarani, Carlo

AU - Triolo, Giovanni

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N2 - Objective: To study the expression of interleukin (IL)-33 and to evaluate its relationship with macrophage polarisation in artery biopsy specimens from patients with giant cell arteritis (GCA). Methods: IL-33, ST2, p-STAT-6 and perivascular IL-1 receptor-associated kinase 1 (p-IRAK1) tissue distribution was evaluated by immunohistochemistry. Inducible nitric oxide synthase and CD163 were also used by immunohistochemistry to evaluate the M1 and M2 polarisation, respectively. Quantitative gene expression analysis of IL-33, T-helper (Th)2-related transcription factor STAT6, Th2 cytokines (IL-4, IL-5, IL-25) and interferon (IFN)-γ was performed in artery biopsy samples obtained from 20 patients with GCA and 15 controls. Five additional patients who had received prednisone when the temporal artery biopsy was performed were also enrolled. Results: IFN-γ and IL-33 were significantly overexpressed in the in flamed arteries of GCA patients. IL-33 overexpression was not accompanied by a concomitant increase of Th2 cytokines. Neovessels scattered through the inflammatory infiltrates were the main sites of IL-33 expression. The expression of IL-33 receptor ST2 and of p-IRAK1 was also increased in GCA patients. Arteries from glucocorticoid-treated patients had a lower expression of IL-33. IL-33 was accompanied by the expression of p-STAT6 and a clear M2 macrophages polarisation. Conclusions: A role for IL-33 in the inflammation of GCA patients is supported by these findings.

AB - Objective: To study the expression of interleukin (IL)-33 and to evaluate its relationship with macrophage polarisation in artery biopsy specimens from patients with giant cell arteritis (GCA). Methods: IL-33, ST2, p-STAT-6 and perivascular IL-1 receptor-associated kinase 1 (p-IRAK1) tissue distribution was evaluated by immunohistochemistry. Inducible nitric oxide synthase and CD163 were also used by immunohistochemistry to evaluate the M1 and M2 polarisation, respectively. Quantitative gene expression analysis of IL-33, T-helper (Th)2-related transcription factor STAT6, Th2 cytokines (IL-4, IL-5, IL-25) and interferon (IFN)-γ was performed in artery biopsy samples obtained from 20 patients with GCA and 15 controls. Five additional patients who had received prednisone when the temporal artery biopsy was performed were also enrolled. Results: IFN-γ and IL-33 were significantly overexpressed in the in flamed arteries of GCA patients. IL-33 overexpression was not accompanied by a concomitant increase of Th2 cytokines. Neovessels scattered through the inflammatory infiltrates were the main sites of IL-33 expression. The expression of IL-33 receptor ST2 and of p-IRAK1 was also increased in GCA patients. Arteries from glucocorticoid-treated patients had a lower expression of IL-33. IL-33 was accompanied by the expression of p-STAT6 and a clear M2 macrophages polarisation. Conclusions: A role for IL-33 in the inflammation of GCA patients is supported by these findings.

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