The absence of functional dectin-1 on enterocytes may serve to prevent intestinal damage

Enterocytes are exposed to antigens present in the intestinal lumen, like beta-glucans that are carbohydrate structures present not only in the cell wall of yeast and fungi but also in cereals. Beta-glucans are known for their immune modulating properties and we have earlier reported an increased immune response by enterocytes after addition of fecal water prepared from ileostomic contents obtained from participants consuming an oat beta-glucan diet versus a placebo diet. We hypothesized that our observation of immune stimulating effects by oat beta-glucan in enterocytes was mediated through the beta-glucan receptor dectin-1.

Presence of dectin-1 in enterocytes was examined by reverse transcriptase PCR, western blot, and flow cytometry followed by an evaluation of the functional involvement of dectin-1 by using dectin-1 inhibitors during fecal water incubations.

Reverse transcriptase PCR and western blot analysis showed dectin-1 presence in the INT407 and Caco-2 NF-kappaB reporter enterocyte cell lines. Moreover, human enterocytes isolated from ileum or colon biopsies also contained dectin-1 protein. However, dectin-1 expression could not be confirmed by flow cytometry in INT407 cells, suggesting that in these cell lines dectin-1 is not expressed at the extracellular membrane. Furthermore, dectin-1 inhibitors did not suppress the beta-glucan containing fecal water-induced IL-8 production by INT407 cells and NF-kappaB transactivation by Caco-2 NF-kappaB reporter cells.

INT407 and Caco-2 NF-kappaB reporter cells seem to express no functional dectin-1. The absence of this pattern recognition receptor may function to protect the intestine against inflammatory damage, as the dectin-1 ligand beta-glucan is largely present in the intestinal lumen.