The Altered Mucosal Barrier Function in the Duodenum Plays a Role in the Pathogenesis of Functional Dyspepsia
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An altered gastrointestinal barrier function is reportedly associated with the pathogenesis of functional dyspepsia (FD); however, the pathogenesis of FD has not yet been fully elucidated.
The objective of the present study was to determine whether the mucosal barrier function is impaired in patients with FD and to investigate the mechanisms underlying FD.
The present study included patients with FD (FD group, n = 24), non-FD patients with abdominal symptoms (symptomatic control group, n = 14), and patients with no abdominal symptoms (asymptomatic control group, n = 20). The groups were compared regarding the mucosal electrical impedance (MI) values of the stomach and duodenum, which were measured using a tissue conductance meter during esophagogastroduodenoscopy.
There were no significant differences between the three groups in the MI of the stomach. In contrast, the duodenal MI of the FD group (17.8 ± 4.3 Ω) was significantly lower than those of the symptomatic control group (27.2 ± 6.4 Ω, p < 0.0001) and asymptomatic control group (23.0 ± 7.4 Ω, p = 0.016). The expression of zonula occludens-1 (ZO-1) was significantly lower in the FD group than in the symptomatic control group (p = 0.011), where ZO-1 was positively correlated with the duodenal MI (β = 0.513, p = 0.017). The interleukin (IL)-1β expression was significantly higher in the FD group than in the symptomatic control group (p = 0.041), where IL-1β was inversely correlated with the duodenal MI (β = − 0.600, p = 0.004).
The mucosal barrier function of the duodenum was altered in patients with FD. Both a decreased ZO-1 and increased IL-1β may play a role in the pathogenesis of FD.
KeywordsFunctional dyspepsia Tight junction Mucosal barrier function Impedance IL-1β ZO-1
We appreciate the technical assistance we received from the Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences. We thank Kelly Zammit, BVSc, from Edanz Editing (www.edanzediting.com/ac), for editing a draft of this manuscript.
KK and HO proposed the study. KK, EI, and YM performed the research. KK and YM collected and analyzed the data. TS, MF, and YO performed the histological diagnosis. KK and EI wrote the manuscript. YO supervised the study. All authors contributed to the interpretation of the study.
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Conflict of interest
The authors declare that they have no conflict of interest.