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P055 Interleukin-7 in aortic adventitia of patients with rheumatoid arthritis and coronary artery disease
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  1. AN Burska1,
  2. K Sime2,
  3. A Williams2,
  4. K Mikkelsen3,
  5. K Saatvedt4,
  6. SM Almdahl5,
  7. I Risnes6,
  8. SE Rynning6,
  9. C Goodyear7,
  10. I Hollan8,9,
  11. F Ponchel1
  1. 1Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds
  2. 2Division of Infection and immunity, Cardiff University School of Medicine, Cardiff, UK
  3. 3Lillehammer Hospital for Rheumatic Diseases, Lillehamer
  4. 4Department of cardiothoracic surgery, Oslo University Hospital, Oslo
  5. 5Department of cardiothoracic surgery, University Hospital of North-Norway, Tromsø
  6. 6Department of cardiothoracic surgery, Feiring Heart Clinic, Feiring, Norway
  7. 7Institute of Infection, Immunity and inflammation, University of Glasgow, Glasgow, UK
  8. 8Department of Medicine, Brigham and Women’s Hospital, Boston, USA
  9. 9Department of Research, Innlandet Hospital Trust, Brumunddal, Norway

Abstract

Introduction Rheumatoid Arthritis (RA) patients have increased cardiovascular risk (CV) due to accelerated atherosclerosis (ATS), which significantly contributes to excess mortality in RA.1 The increased CV risk cannot be fully explained by traditional risk factors and systemic chronic inflammation appears to play a crucial role. Interestingly, IL-7, a proinflammatory cytokine involved in RA pathogenesis, appears to play a role also in ATS2 but its effect on cardiovascular disease (CVD) in RA has not been studied yet.

Objectives To examine serum IL-7 levels and expression of IL-7, IL-7R, CD3 and CD20 in aortic adventitia of RA and non-RA patients with coronary artery disease (CAD) and to search for relationships between systemic IL-7 levels and expression of vascular markers, cardiovascular risk factors including metabolic and inflammatory parameters.

Methods We examined 19 RA and 20 non-RA patients undergoing coronary artery bypass graft surgery included in the Feiring Heart Biopsy Study. Serum IL-7 levels were measured by chemiluminescence (MSD). Biopsies from the adventitia of thoracic aorta from a subset of patients (12 RA and 14 non-RA) were stained for IL-7, IL-7R, CD3 and CD20 by immunohistochemistry and scored per mm2 of tissue.

Results Non-RA patients had lower IL-7 serum levels than RA (3.4±3.3 vs. 6.7±3.5, p<0.05). Independently of RA diagnosis, IL-7 significantly correlated with CRP (rho=0.450, p=0.008), triglycerides (TG, rho=0.566, p=0.005), glucose (rho=0.642, p=0.001) and hypertension (p=0.036). Levels of IL-7 were associated with New York Heart Association class (rho=0.429, p=0.014) and this was stronger in non-RA patients (rho=0.577, p=0.010). No associations were found with smoking or markers of CVD severity (i.e., numbers of arteries with stenosis or previous myocardial infarcts (MI)). The number of IL-7 +and IL-7R+cells/mm2 in adventitia were significantly higher in RA (134.2±45.5 and 144±49.9 respectively) than non-RA patients (46.9±22.8 and 54.4±20.2, p<0.005) and were associated with serum IL-7 levels (rho=0.551 and rho=0.588, p<0.01). Both IL-7 +and IL7R+cells were associated with a positive history of MI (p=0.047 and p=0.005) and IL-7R+cells with the number of previous MIs (rho=0.408, p=0.038). Only in RA patients, IL-7R+cells showed a trend for correlation with TG (rho=0.771, p=0.072). IL-7 +and IL-7R+cells correlated with CD3 (rho=0.688, p=0.013 and rho=0.630, p=0.028), but no correlation was found with CD20. Cholesterol and HDL levels were associated with IL-7 +cells only in non-RA patients (rho=0.729, p=0.04 and rho=0.733, p=0.038).

Conclusions Among patients with CAD, those with RA had higher serum IL-7 and a greater expression of both IL-7 and IL-7R is aortic adventitia. Systemic levels of IL-7 were related to its vascular expression. Thus, the IL-7/IL-7R axis may play a role in the accelerated ATS observed in RA; further studies are needed to elucidate the precise role of IL-7 in CV risk in RA.

References

  1. . Kaplan MJ. Curr. Opin. Rheumatol2006;18(3):289–297.

  2. . Damås JK, et al. Circulation2003;107(21):2670–2676.

Acknowledgements None.

Disclosure of interest None declared

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