Periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis syndrome is linked to dysregulated monocyte IL-1β production

J Allergy Clin Immunol. 2013 Jun;131(6):1635-43. doi: 10.1016/j.jaci.2012.07.043. Epub 2012 Sep 21.

Abstract

Background: The exact pathogenesis of the pediatric disorder periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis (PFAPA) syndrome is unknown.

Objectives: We hypothesized that PFAPA might be due to dysregulated monocyte IL-1β production linked to genetic variants in proinflammatory genes.

Methods: Fifteen patients with PFAPA syndrome were studied during and outside a febrile episode. Hematologic profile, inflammatory markers, and cytokine levels were measured in the blood. The capacity of LPS-stimulated PBMCs and monocytes to secrete IL-1β was assessed by using ELISA, and active IL-1β secretion was visualized by means of Western blotting. Real-time quantitative PCR was performed to assess cytokine gene expression. DNA was screened for variants of the MEFV, TNFRSF1A, MVK, and NLRP3 genes in a total of 57 patients with PFAPA syndrome.

Results: During a febrile attack, patients with PFAPA syndrome revealed significantly increased neutrophil counts, erythrocyte sedimentation rates, and C-reactive protein, serum amyloid A, myeloid-related protein 8/14, and S100A12 levels compared with those seen outside attacks. Stimulated PBMCs secreted significantly more IL-1β during an attack (during a febrile episode, 575 ± 88 pg/mL; outside a febrile episode, 235 ± 56 pg/mL; P < .001), and this was in the mature active p17 form. IL-1β secretion was inhibited by ZYVAD, a caspase inhibitor. Similar results were found for stimulated monocytes (during a febrile episode, 743 ± 183 pg/mL; outside a febrile episode, 227 ± 92 pg/mL; P < .05). Genotyping identified variants in 15 of 57 patients, with 12 NLRP3 variants, 1 TNFRSF1A variant, 4 MEFV variants, and 1 MVK variant.

Conclusion: Our data strongly suggest that IL-1β monocyte production is dysregulated in patients with PFAPA syndrome. Approximately 20% of them were found to have NLRP3 variants, suggesting that inflammasome-related genes might be involved in this autoinflammatory syndrome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Child
  • Female
  • Fever / genetics
  • Fever / immunology
  • Fever / metabolism*
  • Genetic Variation
  • Humans
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation Mediators / blood
  • Interleukin 1 Receptor Antagonist Protein / metabolism
  • Interleukin-1beta / biosynthesis*
  • Leukocyte Count
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / metabolism
  • Lipopolysaccharides / immunology
  • Lymphadenitis / genetics
  • Lymphadenitis / immunology
  • Lymphadenitis / metabolism*
  • Male
  • Middle Aged
  • Monocytes / immunology
  • Monocytes / metabolism*
  • Neutrophils
  • Pharyngitis / genetics
  • Pharyngitis / immunology
  • Pharyngitis / metabolism*
  • Stomatitis, Aphthous / genetics
  • Stomatitis, Aphthous / immunology
  • Stomatitis, Aphthous / metabolism*
  • Syndrome
  • Young Adult

Substances

  • Inflammation Mediators
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1beta
  • Lipopolysaccharides