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  1. L A Simms1,
  2. J D Doecke2,
  3. G L Radford-Smith3
  1. 1
    Queensland Institute of Medical Research, Brisbane, Australia
  2. 2
    Australian E-Health Research Centre, CSIRO Mathematical and Information Sciences, Brisbane, Australia
  3. 3
    Department of Gastroenterology, Royal Brisbane and Women’s Hospital, Brisbane, Australia
  1. L A Simms, Queensland Institute of Medical Research, Brisbane 4006, Australia; Lisa.Simms{at}

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We thank the editors of Gut for the opportunity to respond to the letter of Bevins et al.

The hypothesis by Wehkamp et al1 2 that human α-defensin reduction is linked to NOD2 mutation has until now remained untested by an independent group of investigators. The key issues at variance between our study3 and those of Bevins and colleagues1 2 are (1) whether α-defensin levels are decreased in non-inflamed ileal tissue of patients with Crohn’s disease (CD), and (2) whether a reduction in α-defensins is linked to a mutation in NOD2, specifically SNP13, in patients with ileal CD. This is clinically important as patients with CD with a NOD2 mutation could potentially be treated with an oral administration of natural or recombinant α-defensins. In their letter, Bevins et al raise a number of points.

First, they suggest that decreased Paneth cell defensin expression is linked primarily to the NOD2 SNP13 (1007fs) genotype. In our manuscript we did not present data stratified by 1007fs NOD2 genotype because of the low numbers (n = 8, which is equivalent to their study).2 DEFA5 and DEFA6 in non-inflamed biopsies from patients with ileal CD did not correlate with SNP13 NOD2 genotype (without adjustment for confounders (villin 1 (VIL1) and interleukin 6 (IL6)), DEFA5 p = 0.336, DEFA6 p = 0.316; with adjustment for confounders (VIL1, IL6), DEFA5 p = 0.650, DEFA6 p = 0.471). This finding is consistent for DEFA5 mRNA expression levels normalised to β2-microglobulin (B2M) and to a second …

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  • Competing interests: None.

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