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Open AccessArticle

Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by Campylobacter jejuni

1
Institute of Clinical Physiology/Nutritional Medicine, Medical Department, Division of Gastroenterology, Infectiology, Rheumatology, Charité–Universitätsmedizin Berlin, 12203 Berlin, Germany
2
Institute of Microbiology, Infectious Diseases and Immunology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, 14195 Berlin, Germany
3
Medical Department, Division of Gastroenterology, Infectiology and Rheumatology, Charité–Universitätsmedizin Berlin, 12203 Berlin, Germany
4
German Federal Institute for Risk Assessment (BfR), Department of Biological Safety, National Reference Laboratory for Campylobacter, 12277 Berlin, Germany
5
University of Veterinary Medicine Hannover, Research Center for Emerging Infections and Zoonoses, 30559 Hannover, Germany
6
Institute for Veterinary Food Science, Justus-Liebig-University, 35392 Giessen, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(19), 4830; https://doi.org/10.3390/ijms20194830
Received: 5 August 2019 / Revised: 19 September 2019 / Accepted: 26 September 2019 / Published: 28 September 2019
(This article belongs to the Special Issue The Tight Junction and Its Proteins: More Than Just a Barrier)
Campylobacter jejuni (C. jejuni) is the most common cause of foodborne gastroenteritis worldwide. The bacteria induce diarrhea and inflammation by invading the intestinal epithelium. Curcumin is a natural polyphenol from turmeric rhizome of Curcuma longa, a medical plant, and is commonly used in curry powder. The aim of this study was the investigation of the protective effects of curcumin against immune-induced epithelial barrier dysfunction in C. jejuni infection. The indirect C. jejuni-induced barrier defects and its protection by curcumin were analyzed in co-cultures with HT-29/B6-GR/MR epithelial cells together with differentiated THP-1 immune cells. Electrophysiological measurements revealed a reduction in transepithelial electrical resistance (TER) in infected co-cultures. An increase in fluorescein (332 Da) permeability in co-cultures as well as in the germ-free IL-10−/− mouse model after C. jejuni infection was shown. Curcumin treatment attenuated the C. jejuni-induced increase in fluorescein permeability in both models. Moreover, apoptosis induction, tight junction redistribution, and an increased inflammatory response—represented by TNF-α, IL-1β, and IL-6 secretion—was observed in co-cultures after infection and reversed by curcumin. In conclusion, curcumin protects against indirect C. jejuni-triggered immune-induced barrier defects and might be a therapeutic and protective agent in patients. View Full-Text
Keywords: Campylobacter jejuni; curcumin; tight junction; claudin; apoptosis; co-culture; mouse colon; cytokines; TNF; NFκB Campylobacter jejuni; curcumin; tight junction; claudin; apoptosis; co-culture; mouse colon; cytokines; TNF; NFκB
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Lobo de Sá, F.D.; Butkevych, E.; Nattramilarasu, P.K.; Fromm, A.; Mousavi, S.; Moos, V.; Golz, J.C.; Stingl, K.; Kittler, S.; Seinige, D.; Kehrenberg, C.; Heimesaat, M.M.; Bereswill, S.; Schulzke, J.-D.; Bücker, R. Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by Campylobacter jejuni. Int. J. Mol. Sci. 2019, 20, 4830.

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