Barrier dysfunction is a primary defect in Crohn’s disease (CD). The dysregulated barrier may be explained by the influence of genetics. This was shown by Keita et al. in a study with monozygotic and dizygotic twins who were discordant for CD [16]. A significant increase was observed in gut paracellular permeability in healthy monozygotic twins. It was also demonstrated that the passage of E. coli K-12 could be a consequence of inflammation rather than representing a primary defect in itself.
A total of 15 twin pairs (monozygotic n=9, dizygotic n=6) and ten external controls were included. Healthy co-twins and CD twins displayed increased 51Cr-EDTA permeability at 120 min both with (P<0.001) and without acetylsalicylic acid (P<0.001) compared to the control group. The observed difference took place at 20 min with acetylsalicylic acid when healthy co-twins were compared with external controls (P<0.05). When stratified by zygosity, an increased permeability at 20 min both with (P=0.05) and without acetylsalicylic acid (P<0.05) was observed in healthy monozygotic co-twins.
There were no statistical differences between the healthy dizygotic co-twins and external controls. Healthy monozygotic twins displayed an increased permeability at 20 min without acetylsalicylic acid when compared with healthy dizygotic co-twins (P<0.05). No difference in E. coli passage was observed between groups. Immunofluorescence of the tight junction proteins claudin-5 and tricellulin showed lower levels in healthy co-twins (P<0.05) and CD twins (P<0.05) compared with external controls. Only lower tricellulin in CD was seen compared with controls, however (P<0.05).
- Keita
V, et al. OP001. ECCO 2018.
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