Resistin-like molecule β (RELMβ) is an epithelial cell-specific molecule that has been implicated in the defense against intestinal nematode infections in mice (1, 2). Expression of RELMβ also is induced by bacterial colonization in mice (3) and production appears to be restricted to goblet cells in the lung and the intestinal tract (4). Targeted disruption of the gene encoding RELMβ in mice (Retnlb) reduces the severity of acute colitis induced by dextran sodium sulfate (5).
In the November 15, 2007 issue of The Journal of Immunology, Barnes et al. (6) showed that induction of ileal RELMβ expression is associated with the onset and development of inflammation in SAMP1/Fc mice, a murine model of spontaneous chronic ileitis. The authors subsequently suggested that this molecule could be one of the key mediators in the pathogenesis of Crohn’s disease, an inflammatory bowel disease (IBD) in humans.
However, caution should be exercised when extrapolating the function of a given molecule from mice to humans. We have determined RELMβ expression by real-time RT-PCR in a large number of intestinal biopsies obtained from patients with IBD and did not observe any significant difference between patients with Crohn’s disease and controls, nor between patients with ulcerative colitis and controls.
Furthermore, the gene was expressed at a similar level in both endoscopically normal and inflamed mucosa in the patients. Thus, in contrast to its involvement in the IBD-like disease induced in mice, an altered expression level of RELMβ is not associated with IBD in humans.