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Abstract
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.
Highlights
Campylobacter jejuni is the most prevalent pathogenic bacterium of zoonotic gastroenteritis [1]
Tight junctions form a barrier for water, ions, and solutes [9] and consist of various molecular transmembrane proteins like claudins and occludin, junction adhesion molecules (JAM), tricellulin, and cytoplasmatic scaffolding proteins as zonula occludens protein-1 (ZO-1) [8,9]
No bacteria could be cultured after the experiment, indicating that the bacteria could not pass the filter membrane with 0.4 μm pore size
Summary
Campylobacter jejuni is the most prevalent pathogenic bacterium of zoonotic gastroenteritis [1]. Typical symptoms provoked by C. jejuni are watery to bloody diarrhea, abdominal pain, fever, and nausea [2] This human pathogen is present in the intestinal microbiota of farm animals, especially poultry, which is the main source of infection for humans by ingestion of contaminated or undercooked food [1]. Epithelial lesions can go along with single-cell lesions by increased apoptosis, mid-sized leaks like focal leaks, as well as erosions or even ulcerations These pathological findings could explain the type of diarrhea for the Campylobacter infection as leak flux pathomechanism, which is characterized by a loss of water and solutes from the organism into the intestinal lumen through a leaky epithelium [6,7]. Tight junctions form a barrier for water, ions, and solutes (barrier function) [9] and consist of various molecular transmembrane proteins like claudins and occludin, junction adhesion molecules (JAM), tricellulin, and cytoplasmatic scaffolding proteins as zonula occludens protein-1 (ZO-1) [8,9]
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