The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome

R. Meliconi, M. Uguccioni, F. Chieco-Bianchi, C. Pitzalis, S. Bowman, A. Facchini, G. Gasbarrini, G. S. Panayi, G. H. Kingsley

Research output: Contribution to journalArticle

Abstract

Objective. Felty's syndrome (FS) is defined as rheumatoid arthritis (RA) with neutropenia and, in some cases, splenomegaly; the outcome is primarily determined by the risk of infection, which is related to the degree of neutropenia. We analysed whether the clinical manifestations of FS, especially neutropenia, could be explained by abnormalities in cytokine production. Methods. We examined the production in FS of five cytokines involved in the maturation and activation of polymorphonuclear cells (pMNs): IL-1β, TNFα, IL-8, G-CSF and GM-CSF. Because of the role of systemic IL-8 in neutrophil migration, serum IL-8 levels were also evaluated. Results. Spontaneous and anti-CD16 stimulated cytokine production was similar in FS, RA and healthy controls (NC). However, anti-CD3 stimulated IL-8 production was significantly increased compared to NC in both RA and FS. FS patients who spontaneously produced G-CSF in culture were protected from bacterial infections. Serum IL-8 levels were elevated in FS and RA compared to NC (p <0.001 for both groups). In FS, serum IL-8 was higher in patients with a history of bacterial infections compared to those without (p <0.01) and there was a weak inverse correlation between neutropenia and serum IL-8 levels (Kendal's tau B = -0.31, p = 0.05). Conclusion. The neutropenia of FS cannot be explained by changes in peripheral blood cytokine production, although changes in the bone marrow microenvironment cannot be excluded. Our data do suggest a possible role for G-CSF and IL-8 in the development of certain FS complications.

Original languageEnglish
Pages (from-to)285-291
Number of pages7
JournalClinical and Experimental Rheumatology
Volume13
Issue number3
Publication statusPublished - 1995

Fingerprint

Felty Syndrome
Interleukin-8
Cytokines
Neutropenia
Rheumatoid Arthritis
Granulocyte Colony-Stimulating Factor
Granulocyte-Macrophage Colony-Stimulating Factor
Serum
Bacterial Infections
Splenomegaly
Interleukin-1
Neutrophils

Keywords

  • cytokines
  • Felty's syndrome
  • neutropenia
  • rheumatoid arthritis

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

Cite this

Meliconi, R., Uguccioni, M., Chieco-Bianchi, F., Pitzalis, C., Bowman, S., Facchini, A., ... Kingsley, G. H. (1995). The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome. Clinical and Experimental Rheumatology, 13(3), 285-291.

The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome. / Meliconi, R.; Uguccioni, M.; Chieco-Bianchi, F.; Pitzalis, C.; Bowman, S.; Facchini, A.; Gasbarrini, G.; Panayi, G. S.; Kingsley, G. H.

In: Clinical and Experimental Rheumatology, Vol. 13, No. 3, 1995, p. 285-291.

Research output: Contribution to journalArticle

Meliconi, R, Uguccioni, M, Chieco-Bianchi, F, Pitzalis, C, Bowman, S, Facchini, A, Gasbarrini, G, Panayi, GS & Kingsley, GH 1995, 'The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome', Clinical and Experimental Rheumatology, vol. 13, no. 3, pp. 285-291.
Meliconi R, Uguccioni M, Chieco-Bianchi F, Pitzalis C, Bowman S, Facchini A et al. The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome. Clinical and Experimental Rheumatology. 1995;13(3):285-291.
Meliconi, R. ; Uguccioni, M. ; Chieco-Bianchi, F. ; Pitzalis, C. ; Bowman, S. ; Facchini, A. ; Gasbarrini, G. ; Panayi, G. S. ; Kingsley, G. H. / The role of interleukin-8 and other cytokines in the pathogenesis of Felty's syndrome. In: Clinical and Experimental Rheumatology. 1995 ; Vol. 13, No. 3. pp. 285-291.
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AU - Meliconi, R.

AU - Uguccioni, M.

AU - Chieco-Bianchi, F.

AU - Pitzalis, C.

AU - Bowman, S.

AU - Facchini, A.

AU - Gasbarrini, G.

AU - Panayi, G. S.

AU - Kingsley, G. H.

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N2 - Objective. Felty's syndrome (FS) is defined as rheumatoid arthritis (RA) with neutropenia and, in some cases, splenomegaly; the outcome is primarily determined by the risk of infection, which is related to the degree of neutropenia. We analysed whether the clinical manifestations of FS, especially neutropenia, could be explained by abnormalities in cytokine production. Methods. We examined the production in FS of five cytokines involved in the maturation and activation of polymorphonuclear cells (pMNs): IL-1β, TNFα, IL-8, G-CSF and GM-CSF. Because of the role of systemic IL-8 in neutrophil migration, serum IL-8 levels were also evaluated. Results. Spontaneous and anti-CD16 stimulated cytokine production was similar in FS, RA and healthy controls (NC). However, anti-CD3 stimulated IL-8 production was significantly increased compared to NC in both RA and FS. FS patients who spontaneously produced G-CSF in culture were protected from bacterial infections. Serum IL-8 levels were elevated in FS and RA compared to NC (p <0.001 for both groups). In FS, serum IL-8 was higher in patients with a history of bacterial infections compared to those without (p <0.01) and there was a weak inverse correlation between neutropenia and serum IL-8 levels (Kendal's tau B = -0.31, p = 0.05). Conclusion. The neutropenia of FS cannot be explained by changes in peripheral blood cytokine production, although changes in the bone marrow microenvironment cannot be excluded. Our data do suggest a possible role for G-CSF and IL-8 in the development of certain FS complications.

AB - Objective. Felty's syndrome (FS) is defined as rheumatoid arthritis (RA) with neutropenia and, in some cases, splenomegaly; the outcome is primarily determined by the risk of infection, which is related to the degree of neutropenia. We analysed whether the clinical manifestations of FS, especially neutropenia, could be explained by abnormalities in cytokine production. Methods. We examined the production in FS of five cytokines involved in the maturation and activation of polymorphonuclear cells (pMNs): IL-1β, TNFα, IL-8, G-CSF and GM-CSF. Because of the role of systemic IL-8 in neutrophil migration, serum IL-8 levels were also evaluated. Results. Spontaneous and anti-CD16 stimulated cytokine production was similar in FS, RA and healthy controls (NC). However, anti-CD3 stimulated IL-8 production was significantly increased compared to NC in both RA and FS. FS patients who spontaneously produced G-CSF in culture were protected from bacterial infections. Serum IL-8 levels were elevated in FS and RA compared to NC (p <0.001 for both groups). In FS, serum IL-8 was higher in patients with a history of bacterial infections compared to those without (p <0.01) and there was a weak inverse correlation between neutropenia and serum IL-8 levels (Kendal's tau B = -0.31, p = 0.05). Conclusion. The neutropenia of FS cannot be explained by changes in peripheral blood cytokine production, although changes in the bone marrow microenvironment cannot be excluded. Our data do suggest a possible role for G-CSF and IL-8 in the development of certain FS complications.

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