• C reactive protein
• mesenteric fat
• bacterial translocation
• Crohn's disease
• obesity
• leptin
• IL-18
• chronic IBD
• IBD models
• mucosal immunology

The phenomenon of creeping fat in Crohn's disease (CD), characterised by a hypertrophy of the mesenteric fat surrounding inflamed intestinal segments, was first described by Burrill B Crohn himself at the beginning of the past century.1 An MRI study confirmed this specific finding only a decade ago.2 Nonetheless, the functional impact remained to be elucidated. The fat tissue was solely considered as a storage and endocrine organ for a long time; two parallel developments triggered a paradigm shift: First, in vitro and in vivo studies provided evidence that adipokines released by adipocytes are critical in the regulation of the immune system.3 Furthermore, preadipocytes and adipocytes were found to express functional receptors of the innate immune system. Second, obesity, and in particular excess visceral adipose tissue (VAT), has been identified as a risk factor for cardiovascular diseases and metabolic disorders.4 Here the VAT releases proinflammatory mediators and is also infiltrated by proinflammatory macrophages. Modern concepts consequently define obesity as a state of chronic inflammation.5

A first study by Peyrin-Biroulet et al addresses the specific role of the mesenteric fat in CD (see page 78); the second work by Zulian et al provides a broad expression analysis from fat tissues of different sites from patients with CD as well as from obese and healthy subjects (see page 86).6 7 Synergising each other, these results allow for a better understanding of …