Identification,Probiotic Characterization and Anti-Helicobac
发布时间：2021-12-18 15:19
幽门螺杆菌是引起慢性胃炎,十二指肠溃疡和胃肿瘤的病原体。它悄无声息地潜藏在世界50%的人口,是癌症的主要诱因。抗幽门螺杆菌菌株的出现是治疗感染的又一挑战。然而即使感染得到治疗,复发也是一个普遍的问题。乳酸菌(LAB)的功效已被广泛研究,用于对包括幽门螺杆菌感染在内的多种疾病的治疗产生有益影响。具有潜在益生菌特性的乳酸杆菌是有效用作多种疾病的有益治疗剂。益生菌对病原体的作用涉及不同的机制,包括免疫调节,竞争性排斥,抗菌素的分泌,微生物群的恢复。益生菌的作用是特异性的,与每个菌株特性有关,因此,研究单个菌株的功效至关重要。除了慢性炎症和氧化应激反应,幽门螺杆菌还能引起胃微生物群失衡。益生菌能改善幽门螺杆菌引起的炎症的功效已被广泛研究,而益生菌恢复胃微生物群功效的研究却很少。这项研究的重点是使用预处理和研究新鉴定的副干酪乳杆菌ZFM54菌株在幽门螺杆菌感染的小鼠模型中改善幽门螺杆菌介导的炎症和胃营养不良的潜力。从健康婴儿的粪便中分离出副干酪乳杆菌ZFM54菌株,进行抗幽门螺杆菌潜能测定,并进行全基因组测序。副干酪乳杆菌ZFM54具有益生菌相关性,这些基因具有潜在的益生菌特性,表现在无论是在恶...
【文章来源】： 浙江工商大学浙江省
【文章页数】：149 页
【文章目录】：
摘要
ABSTRACT
ABBREVIATIONS
CHAPTER 1 INTRODUCTION
1.1 INTRODUCTION
1.2 AIMS AND OBJECTIVES
CHAPTER 2 LITERATURE REVIEW
2.1 HELICOBACTER PYLORI:PATHOGENESIS
2.1.1 Epidemiology
2.1.2 Diagnosis
2.1.2.1 Non-invasive methods
2.1.2.2 Urea Breath Test(UBT)
2.1.2.3 Stool antigen test
2.1.2.4 Serology
2.1.2.5 Invasive tests
2.1.2.5.1 Endoscopy and biopsy
2.1.3 Treatment
2.1.3.1 First line of therapy
2.1.3.2 Second line of therapy
2.1.3.3 Third line of therapy
2.2 DEFENCE MECHANISM OF THE HOST
2.2.1 Microbiota as first line of defence
2.2.1.1 Role of microbiota
2.2.1.2 Dysbiosis
2.2.1.3 Gastric microbiota and H.pylori
2.2.1.4 Gastrointestinal epithelium as second line of defence
2.2.3 Immune system as third line of defence
2.2.3.1 Innate and adaptive immune system(Overview)
2.3 HUMAN STOMACH
2.4 HISTORY OF PROBIOTICS
2.4.1 PROBIOTIC
2.4.2 The genus Lactobacillus
2.4.3 Immune tolerance and immune regulation mechanism of Lactic acid bacteria(General overview)
2.5 MECHANISMS OF ACTION OF PROBIOTICS AGAINST HELICOBACTERPYLORI
2.5.1 Immunomodulation
2.5.2 Co-aggregation and aggregation
2.5.3 Strengthening the mucosal barrier
2.5.4 Competition for adhesion
2.5.5 Secretion of antimicrobials
2.6 EXPERIMENTAL STUDIES OF ANTI-H.PYLORI ACTIVITY OF PROBIOTICS WITH CELL LINESAND ANIMALS
2.7 CLINICAL STUDIES USING PROBIOTIC IN H.PYLORI ERADICATION
2.7.1 Probiotic as an alternative to antibiotics to eradicate H.pylori
2.7.2 Probiotics as an adjunct to antibiotics to eradicate H.pylori
CHAPTER 3 IDENTIFICATION AND PROBIOTIC CHARACTERIZATION OFLACTOBACILLUS PARACASEI ZFM54
3.1 INTRODUCTION
3.2 MATERIALS AND METHODS:
3.2.1 Bacterial growth conditions
3.2.2 Identification of L.paracasei ZFM54
3.2.3 Phylogenetic analysis
3.2.4 Genome sequence
3.2.5 Genome annotation
3.2.6 In vitro studies on probiotics characteristics
3.2.7 Pathogen inhibition by agar well diffusion assay
3.2.8 Tolerance to different concentrations of salt
3.2.9 Tolerance to simulated gastric juice
3.2.10 Tolerance to bile salts
3.2.11 Auto-aggregation assay
3.2.12 Hydrophobicity
3.2.13 Antibiotic susceptibility
3.2.14 Toxicity in mice
3.3 RESULTS
3.3.1 Identification of L.paracaseiZFM54
3.3.2 Genomic and probiotic features
3.3.3 Pathogen inhibition by agar well diffusion assay
3.3.4 Tolerance to different concentration of salt
3.3.5 Tolerance to simulated gastric juice
3.3.6 Tolerance to bile salts
3.3.7 Auto-aggregation assay
3.3.8 Hydrophobicity
3.3.9 Antibiotic susceptibility
3.3.10 Acute Toxicity in mice
3.4 Discussion
Chapter 4 In vitro studies on anti-Helicobacter pylori activity of L. paracasei ZFM54
4.1 INTRODUCTION
4.2 MATERIALS AND METHODS
4.2.1 Bacterial strains and culture conditions
4.2.2 Agar well diffusion assay
4.2.3 Urease inhibition assay
4.2.4 Co-aggregation assay
4.2.5 Anti-oxidant activity
4.3 RESULTS
4.3.1 Agar well diffusion assay
4.3.2 Urease inhibition assay
4.3.3 Co-aggregation
4.3.4 Anti-oxidant activity
4.4 DISCUSSION
CHAPTER 5 IN VIVO STUDIES ON PREVENTIVE AND THERAPEUTIC EFFECT OF L.PARACASEI ZFM54 ON H.PYLORI INFECTED MICE MODEL
5.1 INTRODUCTION
5.2 MATERIALS AND METHODS
5.2.1 In vivo experiments with mice
5.2.2 Bacterial cultures
5.2.3 Animals:
5.2.4 MDA assay
5.2.5 GSH assay
5.2.6 Histopathology of Gastric Tissues
5.2.7 Real-time PCR
5.2.7.1 Reverse transcription(qPCR) Method
5.2.8 16S rRNA gene sequencing
5.2.9 16S rRNA sequencing analysis for microbiota
5.2.10 Statistical Analyses
5.3 RESULTS
5.3.1 Weight of mice during preventive experiment with 54 and LGG
5.3.2 Histopathology of stomach tissues
5.3.3 MDA and GSH level
5.3.4 Effect of pretreatment with strain54 and LGG on inflammatory cytokines
5.3.5 Linear discriminent effect size(LEfSe)analysis of bacterial taxa in preventiongroups
5.3.6 Relative abundance of genus Helicobacter in prevention groups
5.3.7 Weight of mice during therapeutic experiment with strain54,LGG and Triple Therapy
5.3.8 Histopathology of stomach tissues
5.3.9 MDA and GSH level
MDA
GSH
5.3.10 Effect of treatment with strain54,LGG and triple therapy(TT) oninflammatorycytokines
5.3.11 Linear discriminent effect size(LEfSe)analysis of bacterial taxa in therapeuticgroups
5.3.12 Relative abundance of genus Helicobacter in therapeutic groups
5.4 DISCUSSION
Chapter 6 Conclusions
6.1 Overall conclusion
6.2 Summary of conclusions
6.3 Future prospects
REFERENCES
ACKNOWLEDGEMENTS
Publications
【参考文献】：
期刊论文
[1]Probiotic BIFICO cocktail ameliorates Helicobacter pylori induced gastritis [J]. Hong-Jing Yu,Wei Liu,Zhen Chang,Hui Shen,Li-Juan He,Sha-Sha Wang,Lu Liu,Yuan-Ying Jiang,Guo-Tong Xu,Mao-Mao An,Jun-Dong Zhang. World Journal of Gastroenterology. 2015(21)
[2]Use of probiotics in the fight against Helicobacter pylori [J]. Paolo Ruggiero. World Journal of Gastrointestinal Pathophysiology. 2014(04)
[3]Factors that mediate colonization of the human stomach by Helicobacter pylori [J]. Ciara Dunne,Brendan Dolan,Marguerite Clyne. World Journal of Gastroenterology. 2014(19)
[4]History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer [J]. David Y Graham. World Journal of Gastroenterology. 2014(18)
[5]Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs [J]. Aline Cristina Targa Cadamuro,Ana Flávia Teixeira Rossi,Nathália Maciel Maniezzo,Ana Elizabete Silva. World Journal of Gastroenterology. 2014(06)
[6]A review of Helicobacter pylori diagnosis, treatment, and methods to detect eradication [J]. Elvira Garza-González,Guillermo Ignacio Perez-Perez,Héctor Jesús Maldonado-Garza,Francisco Javier Bosques-Padilla. World Journal of Gastroenterology. 2014(06)
[7]Helicobacter pylori and interleukin-8 in gastric cancer [J]. Ko Eun Lee,Pham Ngoc Khoi,Yong Xia,Jung Sun Park,Young Eun Joo,Kyung Keun Kim,Seok Yong Choi,Young Do Jung. World Journal of Gastroenterology. 2013(45)
[8]Adjuvant probiotics improve the eradication effect of triple therapy for Helicobacter pylori infection [J]. Yi-Qi Du, Tun Su, Jian-Gao Fan, Yu-Xia Lu, Ping Zheng, Xing-Hua Li, Chuan-Yong Guo, Ping Xu, Yan-Fang Gong, Zhao-Shen Li, Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China, Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University, Shanghai 200240, China, Department of Gastroenterology, Tongji Hospital, Tong Ji University, Shanghai 200092, China, Department of Gastroenterology, Shanghai First People’s Hospital, Shanghai 201620, China, Department of Gastroenterology, Shanghai Eighth People’s Hospital, Shanghai 210035, China , Department of Gastroenterology, Shanghai Tenth People’s Hospital, Shanghai 200072, China, Department of Gastroenterology, Shanghai Songjiang Centeral Hospital, Shanghai 201100, China. World Journal of Gastroenterology. 2012(43)
[9]Lactobacillus plantarum B7 inhibits Helicobacter pylori growth and attenuates gastric inflammation [J]. Chompoonut Sunanliganon,Duangporn Thong-Ngam,Somying Tumwasorn,Naruemon Klaikeaw. World Journal of Gastroenterology. 2012(20)
[10]Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4 [J]. Chao Zhou, Feng-Zhen Ma, Xue-Jie Deng, Hong Yuan, Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China. World Journal of Gastroenterology. 2008(32)
本文编号：3542663
【文章来源】： 浙江工商大学浙江省
【文章页数】：149 页
【文章目录】：
摘要
ABSTRACT
ABBREVIATIONS
CHAPTER 1 INTRODUCTION
1.1 INTRODUCTION
1.2 AIMS AND OBJECTIVES
CHAPTER 2 LITERATURE REVIEW
2.1 HELICOBACTER PYLORI:PATHOGENESIS
2.1.1 Epidemiology
2.1.2 Diagnosis
2.1.2.1 Non-invasive methods
2.1.2.2 Urea Breath Test(UBT)
2.1.2.3 Stool antigen test
2.1.2.4 Serology
2.1.2.5 Invasive tests
2.1.2.5.1 Endoscopy and biopsy
2.1.3 Treatment
2.1.3.1 First line of therapy
2.1.3.2 Second line of therapy
2.1.3.3 Third line of therapy
2.2 DEFENCE MECHANISM OF THE HOST
2.2.1 Microbiota as first line of defence
2.2.1.1 Role of microbiota
2.2.1.2 Dysbiosis
2.2.1.3 Gastric microbiota and H.pylori
2.2.1.4 Gastrointestinal epithelium as second line of defence
2.2.3 Immune system as third line of defence
2.2.3.1 Innate and adaptive immune system(Overview)
2.3 HUMAN STOMACH
2.4 HISTORY OF PROBIOTICS
2.4.1 PROBIOTIC
2.4.2 The genus Lactobacillus
2.4.3 Immune tolerance and immune regulation mechanism of Lactic acid bacteria(General overview)
2.5 MECHANISMS OF ACTION OF PROBIOTICS AGAINST HELICOBACTERPYLORI
2.5.1 Immunomodulation
2.5.2 Co-aggregation and aggregation
2.5.3 Strengthening the mucosal barrier
2.5.4 Competition for adhesion
2.5.5 Secretion of antimicrobials
2.6 EXPERIMENTAL STUDIES OF ANTI-H.PYLORI ACTIVITY OF PROBIOTICS WITH CELL LINESAND ANIMALS
2.7 CLINICAL STUDIES USING PROBIOTIC IN H.PYLORI ERADICATION
2.7.1 Probiotic as an alternative to antibiotics to eradicate H.pylori
2.7.2 Probiotics as an adjunct to antibiotics to eradicate H.pylori
CHAPTER 3 IDENTIFICATION AND PROBIOTIC CHARACTERIZATION OFLACTOBACILLUS PARACASEI ZFM54
3.1 INTRODUCTION
3.2 MATERIALS AND METHODS:
3.2.1 Bacterial growth conditions
3.2.2 Identification of L.paracasei ZFM54
3.2.3 Phylogenetic analysis
3.2.4 Genome sequence
3.2.5 Genome annotation
3.2.6 In vitro studies on probiotics characteristics
3.2.7 Pathogen inhibition by agar well diffusion assay
3.2.8 Tolerance to different concentrations of salt
3.2.9 Tolerance to simulated gastric juice
3.2.10 Tolerance to bile salts
3.2.11 Auto-aggregation assay
3.2.12 Hydrophobicity
3.2.13 Antibiotic susceptibility
3.2.14 Toxicity in mice
3.3 RESULTS
3.3.1 Identification of L.paracaseiZFM54
3.3.2 Genomic and probiotic features
3.3.3 Pathogen inhibition by agar well diffusion assay
3.3.4 Tolerance to different concentration of salt
3.3.5 Tolerance to simulated gastric juice
3.3.6 Tolerance to bile salts
3.3.7 Auto-aggregation assay
3.3.8 Hydrophobicity
3.3.9 Antibiotic susceptibility
3.3.10 Acute Toxicity in mice
3.4 Discussion
Chapter 4 In vitro studies on anti-Helicobacter pylori activity of L. paracasei ZFM54
4.1 INTRODUCTION
4.2 MATERIALS AND METHODS
4.2.1 Bacterial strains and culture conditions
4.2.2 Agar well diffusion assay
4.2.3 Urease inhibition assay
4.2.4 Co-aggregation assay
4.2.5 Anti-oxidant activity
4.3 RESULTS
4.3.1 Agar well diffusion assay
4.3.2 Urease inhibition assay
4.3.3 Co-aggregation
4.3.4 Anti-oxidant activity
4.4 DISCUSSION
CHAPTER 5 IN VIVO STUDIES ON PREVENTIVE AND THERAPEUTIC EFFECT OF L.PARACASEI ZFM54 ON H.PYLORI INFECTED MICE MODEL
5.1 INTRODUCTION
5.2 MATERIALS AND METHODS
5.2.1 In vivo experiments with mice
5.2.2 Bacterial cultures
5.2.3 Animals:
5.2.4 MDA assay
5.2.5 GSH assay
5.2.6 Histopathology of Gastric Tissues
5.2.7 Real-time PCR
5.2.7.1 Reverse transcription(qPCR) Method
5.2.8 16S rRNA gene sequencing
5.2.9 16S rRNA sequencing analysis for microbiota
5.2.10 Statistical Analyses
5.3 RESULTS
5.3.1 Weight of mice during preventive experiment with 54 and LGG
5.3.2 Histopathology of stomach tissues
5.3.3 MDA and GSH level
5.3.4 Effect of pretreatment with strain54 and LGG on inflammatory cytokines
5.3.5 Linear discriminent effect size(LEfSe)analysis of bacterial taxa in preventiongroups
5.3.6 Relative abundance of genus Helicobacter in prevention groups
5.3.7 Weight of mice during therapeutic experiment with strain54,LGG and Triple Therapy
5.3.8 Histopathology of stomach tissues
5.3.9 MDA and GSH level
MDA
GSH
5.3.10 Effect of treatment with strain54,LGG and triple therapy(TT) oninflammatorycytokines
5.3.11 Linear discriminent effect size(LEfSe)analysis of bacterial taxa in therapeuticgroups
5.3.12 Relative abundance of genus Helicobacter in therapeutic groups
5.4 DISCUSSION
Chapter 6 Conclusions
6.1 Overall conclusion
6.2 Summary of conclusions
6.3 Future prospects
REFERENCES
ACKNOWLEDGEMENTS
Publications
【参考文献】：
期刊论文
[1]Probiotic BIFICO cocktail ameliorates Helicobacter pylori induced gastritis [J]. Hong-Jing Yu,Wei Liu,Zhen Chang,Hui Shen,Li-Juan He,Sha-Sha Wang,Lu Liu,Yuan-Ying Jiang,Guo-Tong Xu,Mao-Mao An,Jun-Dong Zhang. World Journal of Gastroenterology. 2015(21)
[2]Use of probiotics in the fight against Helicobacter pylori [J]. Paolo Ruggiero. World Journal of Gastrointestinal Pathophysiology. 2014(04)
[3]Factors that mediate colonization of the human stomach by Helicobacter pylori [J]. Ciara Dunne,Brendan Dolan,Marguerite Clyne. World Journal of Gastroenterology. 2014(19)
[4]History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer [J]. David Y Graham. World Journal of Gastroenterology. 2014(18)
[5]Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs [J]. Aline Cristina Targa Cadamuro,Ana Flávia Teixeira Rossi,Nathália Maciel Maniezzo,Ana Elizabete Silva. World Journal of Gastroenterology. 2014(06)
[6]A review of Helicobacter pylori diagnosis, treatment, and methods to detect eradication [J]. Elvira Garza-González,Guillermo Ignacio Perez-Perez,Héctor Jesús Maldonado-Garza,Francisco Javier Bosques-Padilla. World Journal of Gastroenterology. 2014(06)
[7]Helicobacter pylori and interleukin-8 in gastric cancer [J]. Ko Eun Lee,Pham Ngoc Khoi,Yong Xia,Jung Sun Park,Young Eun Joo,Kyung Keun Kim,Seok Yong Choi,Young Do Jung. World Journal of Gastroenterology. 2013(45)
[8]Adjuvant probiotics improve the eradication effect of triple therapy for Helicobacter pylori infection [J]. Yi-Qi Du, Tun Su, Jian-Gao Fan, Yu-Xia Lu, Ping Zheng, Xing-Hua Li, Chuan-Yong Guo, Ping Xu, Yan-Fang Gong, Zhao-Shen Li, Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China, Department of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University, Shanghai 200240, China, Department of Gastroenterology, Tongji Hospital, Tong Ji University, Shanghai 200092, China, Department of Gastroenterology, Shanghai First People’s Hospital, Shanghai 201620, China, Department of Gastroenterology, Shanghai Eighth People’s Hospital, Shanghai 210035, China , Department of Gastroenterology, Shanghai Tenth People’s Hospital, Shanghai 200072, China, Department of Gastroenterology, Shanghai Songjiang Centeral Hospital, Shanghai 201100, China. World Journal of Gastroenterology. 2012(43)
[9]Lactobacillus plantarum B7 inhibits Helicobacter pylori growth and attenuates gastric inflammation [J]. Chompoonut Sunanliganon,Duangporn Thong-Ngam,Somying Tumwasorn,Naruemon Klaikeaw. World Journal of Gastroenterology. 2012(20)
[10]Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4 [J]. Chao Zhou, Feng-Zhen Ma, Xue-Jie Deng, Hong Yuan, Hong-Sheng Ma, Department of Gastroenterology, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China. World Journal of Gastroenterology. 2008(32)
本文编号：3542663
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