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P079. Effect of enteral nutrition on dendritic cell phenotype in children with Crohn's disease

R. Vora1, D. Bernardo1, J. Fell2, H.O. Al-Hassi1, S.C. Knight1, A.L. Hart3, 1Imperial College London, Antigen Presentation Research Group (APRG), London, United Kingdom, 2Chelsea and Westminster Hospital Foundation NHS Trust, Paediatric Gastroenterology, London, United Kingdom, 3St Mark's Hospital, Colorectal Surgery & IBD Unit, London, United Kingdom


Studies in children have shown exclusive enteral nutrition (EN) to be as effective as steroids in inducing remission in active Crohn's disease (CD) [1]. Animal models of intestinal inflammation and studies in humans with inflammatory bowel disease (IBD) suggest an early and key role for dendritic cells (DC) in initiating intestinal inflammation, in particular with enhanced expression of the activation marker CD40, and the bacterial pattern recognition markers TLR2 & 4 on intestinal DC. In addition, there is increased expression of gut homing molecule β 7 on blood DC in active CD [2]. The childhood DC phenotype in IBD is unknown and the mechanism of action of EN in inducing remission remains unclear, but may involve modulation of mucosal immunity.


Blood (10ml) samples were collected at diagnosis of CD in 5 children (Time 0) before EN and 3 healthy individuals. Blood samples were also collected after 6 weeks of EN in children with CD (Time 6 weeks). Peripheral blood mononuclear cells (PBMC) were obtained by centrifugation of blood over Ficoll Paque Plus. PBMC were labelled with monoclonal antibodies and acquired on a flow cytometer. DC were identified as HLA−DR+ lineage (CD3, CD14, CD16, CD19, CD34 negative) cells and further identified as myeloid (mDC, CD11c+), and putative plasmacytoid (pDC, CD11c−). Expression of homing markers β7 (gut), CLA (skin), CCR9 (small bowel), CCR7 (lymph node), pattern recognition markers (TLR2 & 4) and activation & maturation (CD40 amp; 86) markers were studied in mDC and pDC. Results were compared with DC from healthy individuals. Statistical analyses were carried out using GrapPad Prism software.


Healthy individuals (n = 3) were compared with children with active treatment-naïve CD (n = 5). The median age was 13 years (range 9–15 years). The Montreal classification was A1L2B1 in 4 patients. The PCDAI at diagnosis was a median of 55 (range 25–65). Post EN, all patients were in remission.

Compared with healthy individuals, childhood treatment-naïve active CD had a greater proportion of blood mDC expressing (mean ± standard deviation [SD]) maturation markers CD40 (36±9 vs 10±2) & CD86 (46±18 vs 14±11), TLR2 (56±17 vs 7±6) & TLR4 (50±11 vs 4±3) and gut homing molecule β7 (38±7 v/s 6±1) (p < 0.05).

Following EN, blood mDC in CD displayed a decreased expression of CD40 & CD86 (11±10), TLR2 & 4 (4±2) and β7 (5±1.5) (p < 0.05). Post EN, levels of these DC markers approached those found in healthy individuals.


Childhood treatment-naïve active CD display an activated DC profile, particularly to bacterial products and an enhanced gut homing phenotype, which is restored with EN to a profile similar to that found in healthy individuals.

1. Levine, A., (2013), Effects of enteral nutrition on Crohn's disease: clues to the impact of diet on disease pathogenesis., Inflamm Bowel Dis, 2013. 19(6): p. 1322–9.

2. Hart, A.L., (2005), Characteristics of intestinal dendritic cells in inflammatory bowel diseases., Gastroenterology, 129(1): p. 50–65.