Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by Campylobacter 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 , a medical plant, and is commonly used in curry powder. The aim of this study was the i...

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Veröffentlicht in:International journal of molecular sciences 2019-09, Vol.20 (19), p.4830
Hauptverfasser: Lobo de Sá, Fábia Daniela, Butkevych, Eduard, Nattramilarasu, Praveen Kumar, Fromm, Anja, Mousavi, Soraya, Moos, Verena, Golz, Julia C, Stingl, Kerstin, Kittler, Sophie, Seinige, Diana, Kehrenberg, Corinna, Heimesaat, Markus M, Bereswill, Stefan, Schulzke, Jörg-Dieter, Bücker, Roland
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Sprache:eng
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Zusammenfassung:( ) 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 , 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 infection. The indirect -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 infection was shown. Curcumin treatment attenuated the -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 -triggered immune-induced barrier defects and might be a therapeutic and protective agent in patients.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms20194830