Editorial (Thematic Issue: Advance of Interactions Between Exogenous Natural Bioactive Peptides and Intestinal Barrier and Immune Responses)

2015 ◽  
Vol 16 (7) ◽  
pp. 574-575 ◽  
Author(s):  
Wenhui Wang ◽  
Qianying Yang ◽  
Zhixun Sun ◽  
Xiyue Chen ◽  
Cong Yang ◽  
...  
2018 ◽  
Vol 19 (10) ◽  
pp. 3003 ◽  
Author(s):  
Debora Giordano ◽  
Claudio Pinto ◽  
Luca Maroni ◽  
Antonio Benedetti ◽  
Marco Marzioni

Cholangiocytes, the epithelial cells lining the bile ducts, represent the unique target of a group of progressive diseases known as cholangiopathies whose pathogenesis remain largely unknown. In normal conditions, cholangiocytes are quiescent and participate to the final bile volume and composition. Following exogenous or endogenous stimuli, cholangiocytes undergo extensive modifications of their phenotype. Reactive cholangiocytes actively proliferate and release a set of proinflammatory molecules, which act in autocrine/paracrine manner mediating the cross-talk with other liver cell types and innate and adaptive immune cells. Cholangiocytes themselves activate innate immune responses against gut-derived microorganisms or bacterial products that reach the liver via enterohepatic circulation. Gut microbiota has been implicated in the development and progression of the two most common cholangiopathies, i.e., primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC), which have distinctive microbiota composition compared to healthy individuals. The impairment of intestinal barrier functions or gut dysbiosis expose cholangiocytes to an increasing amount of microorganisms and may exacerbate inflammatory responses thus leading to fibrotic remodeling of the organ. The present review focuses on the complex interactions between the activation of innate immune responses in reactive cholangiocytes, dysbiosis, and gut permeability to bacterial products in the pathogenesis of PSC and PBC.


2019 ◽  
Author(s):  
Yann Malaisé ◽  
Corinne Lencina ◽  
Christel Cartier ◽  
Maïwenn Olier ◽  
Sandrine Ménard ◽  
...  

Abstract Background Bisphenol A (BPA), one of the highest-volume chemicals produced worldwide, has been identified as an endocrine disruptor. Many peer-reviewing studies have reported adverse effects of low dose BPA exposure, particularly during perinatal period (gestation and/or lactation). We previously demonstrated that perinatal oral exposure to BPA (via gavage of mothers during gestation and lactation) has long-term consequences on immune response and intestinal barrier functions. Due to its adverse effects on several developmental and physiological processes, BPA was removed from consumer products and replaced by chemical substitutes such as BPS or BPF, that are structurally similar and not well studied compare to BPA. Here, we aimed to compare perinatal oral exposure to these bisphenols (BPs) at two doses (5 and 50 mg/kg body weight (BW)/day (d)) on gut barrier and immune system in female offspring mice at adulthood (Post Natal Day PND70). Methods Pregnant female mice were orally exposed to BPA, BPS or BPF at 5 or 50 μg/kg BW/d from 15th day of gravidity to weaning of pups at PostNatal Day (PND) 21. Gut barrier function and the humoral and cellular immune responses of adult offspring (PND70) were analysed at intestinal and systemic levels. Results In female offspring, perinatal oral BP exposure led to adverse effects on intestinal barrier and immune response that were dependant of the BP nature (A, S or F) and dose of exposure. Stronger impacts were observed with BPS at the dose of 5µg/kg BW/d on inflammatory markers in feces associated with an increase of anti-E. coli IgG, revealing a defect of gut barrier. BPA and BPF exposure induced prominent changes at low dose in offspring mice, in term of gut barrier functions and cellular immune responses, provoking an intestinal and systemic Th1/Th17 inflammation. Conclusion These findings provide, for the first time, a comparative study of long-time consequences of BPA, S and F perinatal exposure by oral route in offspring mice. This work warms that it is mandatory to consider immune markers and dose in risk assessment associated to new BPA’s alternatives. Keywords: Bisphenol A, Bisphenol S, Bisphenol F, Immune responses, Perinatal exposure, Intestine, Th1/Th17, immunoglobulin, cytokines


2019 ◽  
Vol 102 (2) ◽  
pp. 929-942 ◽  
Author(s):  
Carlotta Giromini ◽  
Federica Cheli ◽  
Raffaella Rebucci ◽  
Antonella Baldi

2015 ◽  
Vol 129 (7) ◽  
pp. 515-527 ◽  
Author(s):  
Angela L. Man ◽  
Eugenio Bertelli ◽  
Silvia Rentini ◽  
Mari Regoli ◽  
Graham Briars ◽  
...  

This work described how important features of the intestinal barrier change across life. In aging individuals the integrity of the epithelial barrier appear to be partially compromised and immune responses to certain microbial antigen show signs of decline.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Anna Negroni ◽  
Salvatore Cucchiara ◽  
Laura Stronati

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota. Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium.


Marine Drugs ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. 127
Author(s):  
Xing-Wei Xiang ◽  
Xiao-Ling Zhou ◽  
Rui Wang ◽  
Cong-Han Shu ◽  
Yu-Fang Zhou ◽  
...  

Bioactive peptides isolated from marine organisms have shown to have potential anti-inflammatory effects. This study aimed to investigate the intestinal protection effect of low molecular peptides (Mw < 1 kDa) produced through enzymatic hydrolysis of tuna processing waste (tuna bioactive peptides (TBP)) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in BALB/c mice. Here, we randomly divided twenty-four male BALB/c mice into four groups: (i) normal (untreated), (ii) DSS-induced model colitis, (iii) low dose TBP+DSS-treated (200 mg/kg/d), and (iv) high dose TBP+DSS-treated groups (500 mg/kg/d). The results showed that TBP significantly reduced mice weight loss and improved morphological and pathological characteristics of colon tissues. In addition, it increased the activities of antioxidant enzymes (SOD and GSH-Px) and decreased inflammatory factors (LPS, IL-6, and TNF-α) expression. TBP increased the gene expression levels of some tight junction (TJ) proteins. Moreover, TBP increased the short-chain fatty acids (SCFAs) levels and the diversity and imbalance of intestinal flora. Therefore, TBP plays some protective roles in the intestinal tract by enhancing antioxidant and anti-inflammatory abilities of the body, improving the intestinal barrier and metabolic abnormalities, and adjusting intestinal flora imbalance.


Author(s):  
Richard J. Clark ◽  
Thanh Huyen Phan ◽  
Angela Song ◽  
André J. Ouellette ◽  
Anne C. Conibear ◽  
...  

Defensins are key components of both innate and adaptive immune responses to pathogens. Cryptdins are mouse alpha-defensins that are secreted from Paneth cells in the small intestine and have disulfide-stabilised structures and antibacterial activities against both Gram-positive and Gram-negative bacteria. The folding and three-dimensional structures of alpha-defensins are thought to depend on a conserved glycine residue that forms a β-bulge. Here we investigated the role of this conserved glycine at position 19 of cryptdin-4 (Crp4) in terms of the folding, structure and stability. A Crp4 variant with D-Ala at position 19 folded efficiently, was stabilised by a large number of hydrogen bonds, and resisted proteolysis in simulated intestinal fluid. Although a variant with L-Ala at position 19 was able to adopt the correct fold, it showed less efficient folding and was degraded more rapidly than the D-Ala variant. These results demonstrate the key role that glycine residues can have in folding of bioactive peptides and can provide insights to guide design of stable antimicrobial peptides that fold efficiently.


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