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Article

Immune-Mediated Aggravation of the Campylobacter concisus-Induced Epithelial Barrier Dysfunction

Institute of Clinical Physiology/Nutritional Medicine, Medical Department, Division of Gastroenterology, Infectiology and Rheumatology, Charité—Universitätsmedizin Berlin, 12203 Berlin, Germany
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Author to whom correspondence should be addressed.
Academic Editor: Andreas Burkovski
Int. J. Mol. Sci. 2021, 22(4), 2043; https://doi.org/10.3390/ijms22042043
Received: 30 December 2020 / Revised: 9 February 2021 / Accepted: 15 February 2021 / Published: 19 February 2021
(This article belongs to the Special Issue Host–Pathogen Interaction 2.0)
Campylobacter concisus is a human-pathogenic bacterium of the gastrointestinal tract. This study aimed at the contribution of the mucosal immune system in the context of intestinal epithelial barrier dysfunction induced by C. concisus. As an experimental leaky gut model, we used in vitro co-cultures of colonic epithelial cell monolayers (HT-29/B6-GR/MR) with M1-macrophage-like THP-1 cells on the basal side. Forty-eight hours after C. concisus infection, the decrease in the transepithelial electrical resistance in cell monolayers was more pronounced in co-culture condition and 22 ± 2% (p < 0.001) higher than the monoculture condition without THP-1 cells. Concomitantly, we observed a reduction in the expression of the tight junction proteins occludin and tricellulin. We also detected a profound increase in 4 kDa FITC-dextran permeability in C. concisus-infected cell monolayers only in co-culture conditions. This is explained by loss of tricellulin from tricellular tight junctions (tTJs) after C. concisus infection. As an underlying mechanism, we observed an inflammatory response after C. concisus infection through pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) released from THP-1 cells in the co-culture condition. In conclusion, the activation of subepithelial immune cells exacerbates colonic epithelial barrier dysfunction by C. concisus through tricellulin disruption in tTJs, leading to increased antigen permeability (leaky gut concept). View Full-Text
Keywords: Campylobacter concisus; HT-29/B6-GR/MR cells; THP-1 cells; leaky gut model; tricellular tight junction; tricellulin; occludin; claudin; tumor necrosis factor-α (TNF-α); interleukin-1β (IL-1β); interleukin-6 (IL-6) Campylobacter concisus; HT-29/B6-GR/MR cells; THP-1 cells; leaky gut model; tricellular tight junction; tricellulin; occludin; claudin; tumor necrosis factor-α (TNF-α); interleukin-1β (IL-1β); interleukin-6 (IL-6)
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MDPI and ACS Style

Nattramilarasu, P.K.; Lobo de Sá, F.D.; Schulzke, J.-D.; Bücker, R. Immune-Mediated Aggravation of the Campylobacter concisus-Induced Epithelial Barrier Dysfunction. Int. J. Mol. Sci. 2021, 22, 2043. https://doi.org/10.3390/ijms22042043

AMA Style

Nattramilarasu PK, Lobo de Sá FD, Schulzke J-D, Bücker R. Immune-Mediated Aggravation of the Campylobacter concisus-Induced Epithelial Barrier Dysfunction. International Journal of Molecular Sciences. 2021; 22(4):2043. https://doi.org/10.3390/ijms22042043

Chicago/Turabian Style

Nattramilarasu, Praveen K., Fábia D. Lobo de Sá, Jörg-Dieter Schulzke, and Roland Bücker. 2021. "Immune-Mediated Aggravation of the Campylobacter concisus-Induced Epithelial Barrier Dysfunction" International Journal of Molecular Sciences 22, no. 4: 2043. https://doi.org/10.3390/ijms22042043

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