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Profile of soluble cytokine receptors in Crohn’s disease
  1. T Gustot1,
  2. A Lemmers2,
  3. E Louis3,
  4. C Nicaise2,
  5. E Quertinmont2,
  6. J Belaiche3,
  7. S Roland4,
  8. A Van Gossum4,
  9. J Devière1,
  10. D Franchimont1
  1. 1Division of Gastroenterology and Hepato-Pancreatology, Erasme Hospital, Brussels, Belgium, and Laboratory of Experimental Gastroenterology, Free University of Brussels, Belgium
  2. 2Laboratory of Experimental Gastroenterology, Free University of Brussels, Belgium
  3. 3Division of Gastroenterology, CHU, University of Liege, Belgium
  4. 4Division of Gastroenterology and Hepato-Pancreatology, Erasme Hospital, Brussels, Belgium
  1. Correspondence to:
    Dr T Gustot
    Division of Gastroenterology, Erasme University Hospital, Free University of Brussels, 808 Lennik St, 1070 Brussels, Belgium;


Introduction: Soluble cytokine receptors (sCRs) modulate the in vivo activity of cytokines. Deficient sCR production could participate in the pathogenesis and course of Crohn’s disease (CD). The aim of the study was to examine the profile of sCRs in CD patients and their modulation by infliximab and corticosteroids.

Methods: We prospectively examined active CD patients (aCD) treated with either infliximab (n = 21) or corticosteroids (n = 9), CD patients in clinical remission (rCD, n = 20), ulcerative colitis patients (UC, n = 24), and healthy subjects (HS, n = 15). Cultures of colonic biopsies were also examined from CD inflamed (n = 8), CD non-inflamed (n = 7), and healthy mucosa (n = 8). Levels of tumour necrosis factor α (TNF-α), soluble TNF receptor I (sTNFRI), soluble TNF receptor II (sTNFRII), interleukin 1β (IL-1β), soluble IL-1 receptor I (sIL-1RI), soluble IL-1 receptor II (sIL-1RII), IL-6, soluble IL-6 receptor (sIL-6R), and sgp130 were measured using ELISA.

Results: Higher levels of sTNFRI (p<0.05, p<0.01), sTNFRII (p<0.01, p<0.01), sIL-1RI (p<0.05, NS), IL-6 (p<0.01, p<0.01), and sIL-6R (p<0.05, NS) were observed in aCD compared with rCD and HS. Interestingly, sIL-1RII (p<0.05, p<0.01) and sgp130 (p<0.01, p<0.01) were profoundly decreased in aCD compared with rCD and HS, and were negatively correlated with CRP. Deficient production of sIL-1RII was specific to CD (not observed in ulcerative colitis), and was further confirmed at the mucosal level. Infliximab decreased sTNFRII at one and four weeks (p<0.05) and enhanced sIL-6R levels at one week (p<0.05). Corticosteroids increased sIL-1RII levels at one week (p<0.05).

Conclusion: CD is associated with dysregulated production of sCRs. Deficiency in sIL-1RII and sgp130 may be essential to CD pathogenesis. Their replacement through the use of fusion proteins could represent future alternative therapeutic strategies for CD.

  • sCRs, soluble cytokine receptors
  • CD, Crohn’s disease
  • aCD, active CD
  • rCD, clinical remission of CD
  • CDinf, inflamed mucosa of CD patients
  • CDnon-inf, non-inflamed mucosa of CD patients
  • HCM, healthy colonic mucosa
  • CDAI, Crohn’s disease activity index
  • TNF-α, tumour necrosis factor α
  • sTNFRI, soluble TNF receptor I
  • sTNFRII, soluble TNF receptor II
  • IL-1β, interleukin 1β
  • sIL-1RI, soluble IL-1 receptor I
  • sIL-1RII, soluble IL-1 receptor II
  • IL-6, interleukin 6
  • sIL-6R, soluble IL-6 receptor
  • APR, acute phase response
  • CRP, C reactive protein
  • UC, ulcerative colitis
  • aUC, active UC
  • rUC, UC in clinical remission
  • cytokine receptors
  • Crohn’s disease
  • acute phase response
  • sIL-1-RII
  • sgp130

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  • Conflict of interest: None declared.