THE DISEASE SPECTRUM OF HELICOBACTER PYLORI : The Immunopathogenesis of Gastroduodenal Ulcer and Gastric Cancer

Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflam...

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Published in	Annual review of microbiology Vol. 54; no. 1; pp. 615 - 640
Main Authors	Ernst, Peter B, Gold, Benjamin D
Format	Journal Article
Language	English
Published	Palo Alto, CA 94303-0139 Annual Reviews 01.01.2000 4139 El Camino Way, P.O. Box 10139 Annual Reviews, Inc USA
Subjects	Adenocarcinoma - etiology Bacteria Bacteriology Biological and medical sciences Cancer Causes of Duodenal Ulcer - etiology epidemiology Fundamental and applied biological sciences. Psychology Gastroenteritis Genetic aspects Helicobacter Infections - epidemiology Helicobacter Infections - immunology Helicobacter pylori Helicobacter pylori - genetics Helicobacter pylori - pathogenicity Humans Immune system Infections Lymphoma - etiology Microbiology Models, Immunological mucosal immunity Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pediatric gastroenterology Risk factors Stomach Stomach diseases Stomach Neoplasms - etiology Stomach Ulcer - etiology Ulcers United States Stomach Immune response Spirillales Digestive system Pathogenesis Spirillaceae Host agent relation Inflammation Review Infection Pathogenicity Helicobacter pylori Bacteriosis Bacteria
Online Access	Get full text
ISSN	0066-4227 1545-3251
DOI	10.1146/annurev.micro.54.1.615

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Abstract	Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection.
AbstractList	Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection. ▪ Abstract Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection. Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection.Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection. Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection. Ernst and Gold propose that gastroduodenal disease associated with Helicobacter pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate whether the infection results in gastroduodenal ulcers or gastric cancer.
Audience	Academic
Author	Gold, Benjamin D Ernst, Peter B
AuthorAffiliation	Departments of Pediatrics, Microbiology and Immunology and the Sealy Center for Molecular Sciences, University of Texas Medical Branch, Galveston, Texas 77555-0366; e-mail Ben_Gold@oz.ped.emory.edu pernst@utmb.edu Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Emory University School of Medicine, and Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30322; e-mail
AuthorAffiliation_xml	– name: Departments of Pediatrics, Microbiology and Immunology and the Sealy Center for Molecular Sciences, University of Texas Medical Branch, Galveston, Texas 77555-0366; e-mail – name: Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Emory University School of Medicine, and Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30322; e-mail – name: pernst@utmb.edu – name: Ben_Gold@oz.ped.emory.edu
Author_xml	– sequence: 1 givenname: Peter B surname: Ernst fullname: Ernst, Peter B – sequence: 2 givenname: Benjamin D surname: Gold fullname: Gold, Benjamin D
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1050883$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/11018139$$D View this record in MEDLINE/PubMed
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Snippet	Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial... ▪ Abstract Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the... Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial... Ernst and Gold propose that gastroduodenal disease associated with Helicobacter pylori infection is predominantly a result of inappropriately regulated gastric...
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SubjectTerms	Adenocarcinoma - etiology Bacteria Bacteriology Biological and medical sciences Cancer Causes of Duodenal Ulcer - etiology epidemiology Fundamental and applied biological sciences. Psychology Gastroenteritis Genetic aspects Helicobacter Infections - epidemiology Helicobacter Infections - immunology Helicobacter pylori Helicobacter pylori - genetics Helicobacter pylori - pathogenicity Humans Immune system Infections Lymphoma - etiology Microbiology Models, Immunological mucosal immunity Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pediatric gastroenterology Risk factors Stomach Stomach diseases Stomach Neoplasms - etiology Stomach Ulcer - etiology Ulcers
Title	THE DISEASE SPECTRUM OF HELICOBACTER PYLORI : The Immunopathogenesis of Gastroduodenal Ulcer and Gastric Cancer
URI	http://dx.doi.org/10.1146/annurev.micro.54.1.615 https://www.ncbi.nlm.nih.gov/pubmed/11018139 https://www.proquest.com/docview/205885219 https://www.proquest.com/docview/17731365 https://www.proquest.com/docview/72314331
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