scholarly journals Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by Campylobacter jejuni

2019 ◽  
Vol 20 (19) ◽  
pp. 4830 ◽  
Author(s):  
Fábia Daniela Lobo de Sá ◽  
Eduard Butkevych ◽  
Praveen Kumar Nattramilarasu ◽  
Anja Fromm ◽  
Soraya Mousavi ◽  
...  

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.

Molecules ◽  
2018 ◽  
Vol 23 (6) ◽  
pp. 1355 ◽  
Author(s):  
Tee Sim ◽  
Hanis Harith ◽  
Chau Tham ◽  
Nur Md Hashim ◽  
Khozirah Shaari ◽  
...  

2020 ◽  
Vol 11 (2) ◽  
pp. 1230-1234
Author(s):  
Chengcheng Ren ◽  
Qiuxiang Zhang ◽  
Bart J. de Haan ◽  
Marijke M. Faas ◽  
Hao Zhang ◽  
...  

TLR2-signalling lactic acid bacterial strains specifically inhibit PKC-dependent gut epithelial barrier integrity loss but cannot dampen MAPK-dependent epithelial barrier disruption.


2003 ◽  
Vol 307 (2) ◽  
pp. 443-449 ◽  
Author(s):  
Xiaonan Han ◽  
Takashi Uchiyama ◽  
Penny L. Sappington ◽  
Arino Yaguchi ◽  
Runkuan Yang ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Linda Chia-Hui Yu

Intestinal epithelial barrier plays a critical role in the maintenance of gut homeostasis by limiting the penetration of luminal bacteria and dietary allergens, yet allowing antigen sampling for the generation of tolerance. Undigested proteins normally do not gain access to the lamina propria due to physical exclusion by tight junctions at the cell-cell contact sites and intracellular degradation by lysosomal enzymes in enterocytes. An intriguing question then arises: how do macromolecular food antigens cross the epithelial barrier? This review discusses the epithelial barrier dysfunction in sensitized intestine with special emphasis on the molecular mechanism of the enhanced transcytotic rates of allergens. The sensitization phase of allergy is characterized by antigen-induced cross-linking of IgE bound to high affinity FcεRI on mast cell surface, leading to anaphylactic responses. Recent studies have demonstrated that prior to mast cell activation, food allergens are transported in large quantity across the epithelium and are protected from lysosomal degradation by binding to cell surface IgE and low-affinity receptor CD23/FcεRII. Improved immunotherapies are currently under study including anti-IgE and anti-CD23 antibodies for the management of atopic disorders.


2006 ◽  
Vol 12 (9) ◽  
pp. 843-852 ◽  
Author(s):  
Monica Porras ◽  
Maria Teresa Martín ◽  
Ping-Chang Yang ◽  
Jennifer Jury ◽  
Mary H. Perdue ◽  
...  

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