Retraction notice to “Dietary Allium hookeri reduces inflammatory response and increases expression of intestinal tight junction proteins in LPS-induced young broiler chickens” [Research in Veterinary Science 112C (2017) 149–155]

Objective: This study assessed the effects of probiotics on cecal microbiota, gene expression of intestinal tight junction proteins, and immune response in the cecal tonsil of broiler chickens challenged with Salmonella enterica subsp. enterica.Methods: One-day-old broiler chickens (n = 240) were randomly allocated to four treatments: negative control (Cont), multi-strain probiotic-treated group (Pro), Salmonella-infected group (Sal), and multi-strain probiotic-treated and Salmonella-infected group (ProSal). All chickens except those in the Cont and Pro groups were gavaged with 1×10<sup>8</sup> cfu/mL of S. enterica subsp. enterica 4 days after hatching.Results: Our results indicated that body weight, weight gain, and feed conversion ratio of birds were significantly reduced (p<0.05) by Salmonella challenge. Chickens challenged with Salmonella decreased cecal microbial diversity. Chickens in the Sal group exhibited abundant Proteobacteria than those in the Cont, Pro, and ProSal groups. Salmonella infection downregulated gene expression of Occludin, zonula occludens-1 (ZO1), and Mucin 2 in the jejunum and Occludin and Claudin in the ileum. Moreover, the Sal group increased gene expression of interferon-γ (IFN-γ), interleukin-6 (IL-6), IL-1β, and lipopolysaccharide-induced tumor necrosis factor-alpha factor (LITAF) and reduced levels of transforming growth factor-β4 and IL-10 compared with the other groups (p<0.05). However, chickens receiving probiotic diets increased Lactobacillaceae abundance and reduced Enterobacteriaceae abundance in the ceca. Moreover, supplementation with probiotics increased the mRNA expression of Occludin, ZO1, and Mucin 2 in the ileum (p<0.05). In addition, probiotic supplementation downregulated the mRNA levels of IFN-γ (p<0.05) and LITAF (p = 0.075) and upregulated IL-10 (p = 0.084) expression in the cecal tonsil.Conclusion: The administration of multi-strain probiotics modulated intestinal microbiota, gene expression of tight junction proteins, and immunomodulatory activity in broiler chickens.

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Impacts of increasing challenge with Eimeria maxima on the growth performance and gene expression of biomarkers associated with intestinal integrity and nutrient transporters

Veterinary Research ◽

10.1186/s13567-021-00949-3 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Po-Yun Teng ◽

Janghan Choi ◽

Yuguo Tompkins ◽

Hyun Lillehoj ◽

Woo Kim

Keyword(s):

Gene Expression ◽

Amino Acid ◽

Tight Junction ◽

Growth Performance ◽

Broiler Chickens ◽

Nutrient Transporters ◽

Tight Junction Proteins ◽

Intestinal Integrity ◽

Eimeria Maxima ◽

Junction Proteins

AbstractThis study was conducted to investigate the impacts of graded severity of Eimeria maxima infection on the growth performance and intestine health of broiler chickens. Four different levels of E. maxima-challenged treatments were used, including a non-challenged control group, a low challenge (12 500 oocysts), a medium challenge (25 000 oocysts), and a high challenge dose (50 000 oocysts). There were eight replicate cages per treatment, with 12 birds in each cage, and chickens in the challenged groups orally received sporulated oocysts on day 14. Gastrointestinal permeability was measured by fluorescein isothiocyanate dextran at 5 days post-infection (dpi), whereas intestinal morphology and gene expression of nutrient transporters and tight junction proteins were determined at 6 dpi. The results demonstrate a linear reduction in growth performance, jejunal villus height, and jejunal integrity with graded challenge doses of E. maxima (P < 0.01). Moreover, linear regulation of nutrient transporters and tight junction proteins was a consequence of increasing Eimeria infection levels (P < 0.01). The linear increase of Claudin 1, cationic amino acid transporter, glucose transporter 1, and L-type amino acid transporter genes was associated with increased severity of coccidiosis (P < 0.01). Furthermore, expression of nutrient transporters located at the brush border membrane were down-regulated (P < 0.01) with increasing E. maxima inoculation dose. In conclusion, growth performance and key intestinal integrity biomarkers in broiler chickens were adversely influenced in a dose-dependent manner by E. maxima infection.

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Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

Nutrients ◽

10.3390/nu13103315 ◽

2021 ◽

Vol 13 (10) ◽

pp. 3315

Author(s):

Qiuyu Zhang ◽

Lei Cheng ◽

Junjuan Wang ◽

Mengzhen Hao ◽

Huilian Che

Keyword(s):

Food Allergy ◽

Inflammatory Response ◽

Gut Microbiota ◽

Tight Junction ◽

Intestinal Barrier ◽

Later Life ◽

Food Allergies ◽

Tight Junction Proteins ◽

Gut Microbiota Dysbiosis ◽

Junction Proteins

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

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Lactobacillus casei Zhang Counteracts Blood-Milk Barrier Disruption and Moderates the Inflammatory Response in Escherichia coli-Induced Mastitis

Frontiers in Microbiology ◽

10.3389/fmicb.2021.675492 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yuhui Zheng ◽

Gang Liu ◽

Wei Wang ◽

Yajing Wang ◽

Zhijun Cao ◽

...

Keyword(s):

Escherichia Coli ◽

Inflammatory Response ◽

Tight Junction ◽

Lactobacillus Casei ◽

Mammary Tissue ◽

Tight Junction Proteins ◽

E Coli ◽

Tnf Α ◽

Injury Models ◽

Junction Proteins

Escherichia coli is a common mastitis-causing pathogen that can disrupt the blood-milk barrier of mammals. Although Lactobacillus casei Zhang (LCZ) can alleviate mice mastitis, whether it has a prophylactic effect on E. coli-induced mastitis through intramammary infusion, as well as its underlying mechanism, remains unclear. In this study, E. coli-induced injury models of bovine mammary epithelial cells (BMECs) and mice in lactation were used to fill this research gap. In vitro tests of BMECs revealed that LCZ significantly inhibited the E. coli adhesion (p < 0.01); reduced the cell desmosome damage; increased the expression of the tight junction proteins claudin-1, claudin-4, occludin, and zonula occludens-1 (ZO-1; p < 0.01); and decreased the expression of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 (p < 0.01), thereby increasing trans-epithelial electric resistance (p < 0.01) and attenuating the lactate dehydrogenase release induced by E. coli (p < 0.01). In vivo tests indicated that LCZ significantly reduced the injury and histological score of mice mammary tissues in E. coli-induced mastitis (p < 0.01) by significantly promoting the expression of the tight junction proteins claudin-3, occludin, and ZO-1 (p < 0.01), which ameliorated blood-milk barrier disruption, and decreasing the expression of the inflammatory cytokines (TNF-α, IL-1β, and IL-6) in mice mammary tissue (p < 0.01). Our study suggested that LCZ counteracted the disrupted blood-milk barrier and moderated the inflammatory response in E. coli-induced injury models, indicating that LCZ can ameliorate the injury of mammary tissue in mastitis.

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