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Zinc glycine chelate ameliorates DSS‑induced intestinal barrier dysfunction via attenuating TLR4/NF‑κB pathway in meat ducks

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Journal of Animal Science and Biotechnology 2024年第2期15卷 765-778页

作者： Yaqi Chang Ke Wang Guangmang Liu Hua Zhao Xiaoling Chen Jingyi Cai Gang Jia Institute of Animal Nutrition Key Laboratory for Animal Disease‑Resistance Nutrition of ChinaMinistry of EducationSichuan Agricultural UniversityChengdu 611130SichuanChina

Background Zinc glycine chelate(Zn-Gly)has anti-inflammation and growth-promoting properties;however,the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation is unknown.Three-hundred 1-day-old ducks were divided into 5 groups(6 replicates and 10 ducks per replicate)in a completely randomized design:the control and dextran sulfate sodium(DSS)groups were fed a corn-soybean meal basal diet,and experimental groups received supplements of 70,120 or 170 mg/kg Zn in form of Zn-Gly.The DSS and treatment groups were given 2 mL of 0.45 g/mL DSS daily during d 15–21,and the control group received normal saline.The experiment lasted 21 d.Results Compared with DSS group,70,120 and 170 mg/kg Zn significantly increased body weight(BW),villus height and the ratio of villus to crypt,and significantly decreased the crypt depth of jejunum at 21 d.The number of goblet cells in jejunal villi in the Zn-Gly group was significantly increased by periodic acid-Schiff staining.Compared with control,the content of intestinal permeability marker D-lactic acid(D-LA)and fluxes of fluorescein isothiocyanate(FITC-D)in plasma of DSS group significantly increased,and 170 mg/kg Zn supplementation significantly decreased the D-LA content and FITC-D fluxes.Compared with control,contents of plasma,jejunum endotoxin and jejunum pro-inflammatory factors IL-1β,IL-6 and TNF-αwere significantly increased in DSS group,and were significantly decreased by 170 mg/kg Zn supplementation.Dietary Zn significantly increased the contents of anti-inflammatory factors IL-10,IL-22 and sIgA and IgG in jejunum.Real-time PCR and Western blot results showed that 170 mg/kg Zn supplementation significantly increased mRNA expression levels of CLDN-1 and expression of OCLN protein in jejunum,and decreased gene and protein expression of CLDN-2 compared with DSS group.The 120 mg/kg Zn significantly promoted the expressions of IL-22 and IgA.Dietary Zn-Gly supplementation significantly decreased pro-inflammatory genes IL-8

关键词： Cherry Valley ducks Growth performance gut inflammation Intestinal barrier Zn-Gly

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gut microbiota-derived short chain fatty acids are potential mediators in gut inflammation

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Animal Nutrition 2022年第1期8卷 350-360页

作者： Muhammad Akhtar Yan Chen Ziyu Ma Xiaolong Zhang Deshi Shi Jawaria AKhan Huazhen Liu Department of Basic Veterinary Medicine College of Animal Science and Veterinary MedicineHuazhong Agricultural UniversityWuhan430070China Department of Preventive Veterinary Medicine College of Animal Science and Veterinary MedicineHuazhong Agricultural UniversityWuhan430070China Department of Veterinary Medicine Faculty of Veterinary ScienceUniversity of Veterinary and Animal SciencesLahore54000Pakistan

gut inflammation is a challenging concern in humans and animals,which disturbs normal growth and leads to severe bowel diseases.Short chain fatty acids(SCFA)are the gut microbiota metabolites produced from fermentation of non-digestible carbohydrates,and have been reported to modulate gut inflammation.SCFA have been implicated as the potential therapeutic bioactive molecules for gut inflammatory diseases,and could be an alternative to antibiotic growth promoters(AGP).In this review,the existing knowledge about the types of SCFA,the related gut microbes producing SCFA,the roles of SCFA in maintaining gut homeostasis,and how SCFA modulate gut inflammation is summarized.The therapeutic application of SCFA in the treatment of inflammatory bowel disease(IBD)is also highlighted

关键词： gut microbiota Short chain fatty acid gut inflammation gut homeostasis Inflammatory bowel disease

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Non-celiac gluten sensitivity： questions still to be answered despite increasing awareness

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Cellular & Molecular Immunology 2013年第5期10卷 383-392页

作者： Umberto Volta Giacomo Caio Francesco Tovoli Roberto De Giorgio Department of Medical and Surgical Sciences St. Orsola-Malpighi Hospital University of Bologna Bologna Italy

Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defined as non-celiac gluten sensitivity. Our knowledge regarding this syndrome is still lacking, and many aspects of this syndrome remain unknown. Its pathogenesis is heterogeneous, with a recognized pivotal role for innate immunity; many other factors also contribute, inctuding tow-grade intestinal inflammation, increased intestinal barrier function and changes in the intestinal microbiota. Gluten and other wheat proteins, such as amylase trypsin inhibitors, are the primary triggers of this syndrome, but it has also been hypothesized that a diet rich in fermentable monosaccharides and polyols may elicit its functional gastrointestinal symptoms. The epidemiology of this condition is far from established; its prevalence in the general population is highly variable, ranging from 0.63% to 6%. From a clinical point of view, non-celiac gluten sensitivity is characterized by a wide array of gastrointestinal and extraintestinal symptoms that occur shortly after the ingestion of gluten and improve or disappear when gluten is withdrawn from the diet. These symptoms recur when gluten is reintroduced. Because diagnostic biomarkers have not yet been identified, a double-blind placebo-controlled gluten challenge is currently the diagnostic method with the highest accuracy. Future research is needed to generate more knowledge regarding non-celiac gluten sensitivity, a condition that has global acceptance but has only a few certainties and many unresolved issues.

关键词： celiac disease epithelial barrier function gut inflammation non-celiac gluten sensitivity wheat allergy

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Acquired aplastic anemia:Is bystander insult to autologous hematopoiesis driven by immune surveillance against malignant cells?

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World Journal of Stem Cells 2020年第11期12卷 1429-1438页

作者： Xi-Chen Zhao Xiao-Yun Sun Bo Ju Fan-Jun Meng Hong-Guo Zhao Department of Hematology The Central Hospital of Qingdao West Coast New AreaQingdao 266555Shandong ProvinceChina Department of Hematology The Affiliated Hospital of Qingdao UniversityQingdao 266000Shandong ProvinceChina

We previously reported a serendipitous finding from a patient with refractory severe aplastic anemia who had gotten an unexpected hematological response to treatment with gut-cleansing preparations(GCPs).This patient experienced three recurrences over the ensuing one year of intermittent GCP treatments,with each recurrence occurring 7-8 wk from a GCP.After his third recurrence,he was prescribed successive treatment with rifampicin,berberine,and monthly administered GCP for 4 mo,and he developed an erythroid proliferative neoplasma and an overwhelming enteropathy,and eventually died of septic shock.Laboratory investigations had validated the resolution of myelosuppression and the appearance of malignant clonal hematopoiesis.From the treatment process and laboratory investigations,it is reasonably inferred that the engagement of gut inflammation is critically required in sustaining the overall pathophysiology of acquired aplastic anemia probably by creating a chronic inflammatory state.Incorporation of rifampicin,berberine,and monthly GCP into cyclosporine can enhance the immunosuppressive effect.In a subgroup of acquired aplastic anemia patients whose pathogenesis is associated with genotoxic exposure,the suppressed normal hematopoiesis may result from the bystander insult that is mediated by the soluble inflammatory cytokines generated in response to the immunogenic products of damaged hematopoietic cells in the context of chronic inflammatory state and may offer a protective antineoplastic mechanism against malignant proliferation.

关键词： Acquired aplastic anemia Bystander insult Malignant clonal hematopoiesis Immune surveillance Antineoplastic gut inflammation

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Implications of hepatic dysfunction in Kawasaki disease:Time-related changes in aspartate aminotransferase, alanine aminotransferase,total bilirubin,and C-reactive protein levels

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Pediatric Investigation 2019年第1期3卷 19-26页

作者： Yasuhiko Tomita Takashi Fukaya Yasuko Yamaura Rie Tsujiguchi Haruko Muratani Maki Shimaya Hyogo Health Service Association Center for Health Evaluation and PromotionKobeHyogoJapan

Importance:The cause of the hepatic dysfunction that commonly accompanies Kawasaki disease(KD)remains unclear.Objective:We tried to clarify the cause of the hepatic dysfunction.Methods:A total of 381 consecutive patients with acute KD,who had undergone inpatient treatment with intravenous immunoglobulin until the 7th day of illness,were divided into a group of 199 patients with an alanine aminotransferase(ALT)level≥40 IU/L on admission(group I),a group of 52 patients with an ALT level≥40 IU/L at some point after admission(group II),and a group of 130 patients with ALT levels consistentlyinflammation.

关键词： Kawasaki disease Dysbiosis Fecal calprotectin gut inflammation Pathogenesis Portal vein

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