RESUMO
Helicobacter pylori colonizes the human gastric mucosa, causing inflammation that leads to atrophic gastritis, and it can cause peptic ulcer and gastric cancer. We show that polyphenol administration to mice experimentally infected by H. pylori or treated with VacA toxin can limit gastric epithelium damage, an effect that may be linked to VacA inhibition.
Assuntos
Proteínas de Bactérias/administração & dosagem , Flavonoides/uso terapêutico , Gastrite/tratamento farmacológico , Infecções por Helicobacter/tratamento farmacológico , Fenóis/uso terapêutico , Animais , Contagem de Colônia Microbiana , Flavonoides/administração & dosagem , Mucosa Gástrica/microbiologia , Gastrite/microbiologia , Infecções por Helicobacter/microbiologia , Helicobacter pylori/efeitos dos fármacos , Helicobacter pylori/crescimento & desenvolvimento , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Fenóis/administração & dosagem , Polifenóis , Organismos Livres de Patógenos Específicos , Taninos/administração & dosagem , Taninos/uso terapêuticoRESUMO
Experimental infection of beagle dogs with Helicobacter pylori induces recruitment to the gastric mucosae of neutrophils at early stages and later of mononuclear cells that organize into lymphoid follicles. These structures become macroscopically evident and consist of peripheral CD4(+) T lymphocytes and central CD21(+) B lymphocytes. Furthermore, transient expression of interleukin-8 (IL-8) parallels the presence of neutrophils in the gastric mucosae, whereas expression of IL-6 tends to persist chronically.
Assuntos
Mucosa Gástrica/patologia , Infecções por Helicobacter/patologia , Helicobacter pylori , Leucócitos , Tecido Linfoide , Animais , Cães , Mucosa Gástrica/imunologia , Infecções por Helicobacter/imunologia , Leucócitos Mononucleares , NeutrófilosRESUMO
Helicobacter pylori has been widely recognized as an important human pathogen responsible for chronic gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. Little is known about the natural history of this infection since patients are usually recognized as having the infection only after years or decades of chronic disease. Several animal models of H. pylori infection, including those with different species of rodents, nonhuman primates, and germ-free animals, have been developed. Here we describe a new animal model in which the clinical, pathological, microbiological, and immunological aspects of human acute and chronic infection are mimicked and which allows us to monitor these aspects of infection within the same individuals. Conventional Beagle dogs were infected orally with a mouse-adapted strain of H. pylori and monitored for up to 24 weeks. Acute infection caused vomiting and diarrhea. The acute phase was followed by polymorphonuclear cell infiltration, interleukin 8 induction, mononuclear cell recruitment, and the appearance of a specific antibody response against H. pylori. The chronic phase was characterized by gastritis, epithelial alterations, superficial erosions, and the appearance of the typical macroscopic follicles that in humans are considered possible precursors of MALT lymphoma. In conclusion, infection in this model mimics closely human infection and allows us to study those phases that cannot be studied in humans. This new model can be a unique tool for learning more about the disease and for developing strategies for treatment and prevention.