Article Text

AB0222 Monocyte-derived IL-32 expression correlates with the level of inflammation in salivary glands of sjÖgren’s syndrome
  1. W. Murray-Brown1,
  2. G. Picarelli2,
  3. S. Vartoukian3,
  4. N. Sutcliffe4,
  5. F. Fortune3,
  6. G. Valesini2,
  7. C. Pitzalis1,
  8. A. Tappuni3,
  9. R. Priori2,
  10. M. Bombardieri1
  1. 1William Harvey Research Institute, Queen Mary University of London, london, United Kingdom
  2. 2Rheumatology, University La Sapienza, Rome, Italy
  3. 3Oral Medicine
  4. 4Rheumatology, Queen Mary University of London, london, United Kingdom


Background IL-32, a recently described cytokine promoting pro-inflammatory cytokines such as IL-1β, IL-6, CXCL8 and TNFα, has emerged as a key component in the development of chronic inflammatory diseases such as rheumatoid arthritis.

Objectives To we investigate IL-32 expression at transctipt and protein level and identify IL-32 producing cells in the salivary glands (SG) of Sjögren’s Syndrome (SS) patients.

Methods IL-32 mRNA expression level was assessed by Taqman quantitative PCR in SG of SS patients and non-specific chronic sialadenitis (NSCS) as controls. Patients and control were enrolled in two different Centres. In addition, immunohistochemistry was used to assess IL-32 expression and the formation of B/T cell aggregates. Double immunofluorescence for IL-32 and CD68 was used to identify the cellular source of IL-32 in the SG.

Results Expression of IL-32 correlated with the severity of inflammation and was significantly increased in SS patients compared to NSCS controls (mean±SEM; 10.3±2.1 vs 4.1±0.5, p<0.005). In addition, IL-32 mRNA correlated with the levels of CXCL13 (Spearman’s r=0.50, p=0.004), a lymphoid chemokine strictly associated with the formation of B/T cell aggregates. Immunohistochemistry identified IL-32+ cells in periductal aggregates in SS but not in controls. Conversely, both SS and control SG showed abundant IL-32 staining on salivary ductal epithelial cells. Finally, double immunofluorescence identified monocyte-derived CD68+ cells as the main source of IL-32 within lymphoid aggregates in SS.

Conclusions Here we show that IL-32 expression is significantly increased in the SG of SS patients where both ductal epithelial cells and monocyte-derived cells abundantly express this cytokine. These data strongly implicate IL-32 in the maintenance of chronic inflammation in the target organ of SS.

Disclosure of Interest None Declared

Statistics from

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.