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Category: Bacterial Pathogenesis
Helicobacter pylori, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555818104/9781555811594_Chap13-1.gif /docserver/preview/fulltext/10.1128/9781555818104/9781555811594_Chap13-2.gifAbstract:
Helicobacter pylori is extraordinary among bacteria in its ability to colonize the stomachs of more than half of all people worldwide and often to persist for years or decades once it has become established. H. pylori can be detected and analyzed by a variety of different methods. Seroepidemiological studies performed in the United States and abroad have demonstrated the worldwide presence of H. pylori in a large majority of individuals from low socioeconomic groups and also in many people of higher socioeconomic status. The recent observation that H. pylori can be isolated from cats and that cats can be colonized by H. pylori following inoculation suggests that transmission from pets to humans (or humans to pets) is also possible. The presence of H. pylori can be diagnosed from gastric-biopsy specimens harvested at endoscopy. Long-term gastric colonization is associated with intense humoral and cellular immune responses. However, these responses are usually unable to eradicate H. pylori and they may, in fact, play a role in the persistence of the bacterium and/or in the production of disease. Interestingly, vaccination can reduce the severity of antral gastritis in mice, ferrets, and monkeys. However, immunization can eliminate colonization by H. pylori in mice and ferrets but not in monkeys or humans. The immune response to colonization by H. pylori has been proposed as being responsible in part for the production of peptic ulcer disease (PUD).
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Schematic representation of the flow of particles within the stomach lumen (arrows indicate direction of peristaltic waves or flow).
Schematic representation of the flow of particles within the stomach lumen (arrows indicate direction of peristaltic waves or flow).
Time course of antral gastritis score (●) and plasma IgG (▽) before and after transient or unsuccessful colonization. Absence of the organism is indicated by ○, and positivity for H. pylori by culture and/or histology is indicated by +. Animal 9A5 was not colonized in trial 1 but developed transient colonization during trials 2 and 3. Animal 8V5 was not colonized during trials 1 and 2 but developed transient colonization during trial 3. Animal E0E was included only in trial 2 and did not become colonized with H. pylori ( 34 ).
Time course of antral gastritis score (●) and plasma IgG (▽) before and after transient or unsuccessful colonization. Absence of the organism is indicated by ○, and positivity for H. pylori by culture and/or histology is indicated by +. Animal 9A5 was not colonized in trial 1 but developed transient colonization during trials 2 and 3. Animal 8V5 was not colonized during trials 1 and 2 but developed transient colonization during trial 3. Animal E0E was included only in trial 2 and did not become colonized with H. pylori ( 34 ).
Time course of antral gastritis score (●) and plasma IgG (▽) before and after successful colonization. Absence of the organism is indicated by ○, and positivity for H. pylori by culture and/or histology is indicated by +. Animal 8RC became persistently colonized in trial 2, and the plasma IgG and gastritis scores increased after a 3-month delay. Animal KJ2 did not become colonized in trial 2 but was colonized by one of the human strains from a patient with gastric ulcer used in trial 3 ( 34 ).
Time course of antral gastritis score (●) and plasma IgG (▽) before and after successful colonization. Absence of the organism is indicated by ○, and positivity for H. pylori by culture and/or histology is indicated by +. Animal 8RC became persistently colonized in trial 2, and the plasma IgG and gastritis scores increased after a 3-month delay. Animal KJ2 did not become colonized in trial 2 but was colonized by one of the human strains from a patient with gastric ulcer used in trial 3 ( 34 ).
Effect of administration of rUre plus LT or placebo plus LT on conversion in specific antiurease serum and saliva IgG and IgA at 1 week after the fourth immunization. The H. pylori + or − designation reflects the status at endoscopy 11.5 months after immunization. The dotted line represents 100% of the initial immunoglobulin level. *, P < 0.05 ( 36 ). SE, standard error.
Effect of administration of rUre plus LT or placebo plus LT on conversion in specific antiurease serum and saliva IgG and IgA at 1 week after the fourth immunization. The H. pylori + or − designation reflects the status at endoscopy 11.5 months after immunization. The dotted line represents 100% of the initial immunoglobulin level. *, P < 0.05 ( 36 ). SE, standard error.
Time course of serum anti-urease IgG. Following administration of rUre plus LT, mean IgG initially increased (○ and +). IgG subsequently decreased in animals that were H. pylori-negative at the endoscopy performed at 11.5 months (○; n = 8), whereas it did not change significantly in those who were H. pylori positive at 11.5 months (+ ; n = 18). In animals given placebo plus LT, IgG initially did not change and then increased progressively in the animals that were H. pylori positive at the endoscopy performed at 11.5 months (♦; n = 27). IgG remained low in the two animals that had received placebo plus LT and remained H. pylori negative (data not illustrated). *, P < 0.05 versus placebo plus LT and H. pylori positive at 11.5 months. SE, standard error. (Adapted from reference 36 .)
Time course of serum anti-urease IgG. Following administration of rUre plus LT, mean IgG initially increased (○ and +). IgG subsequently decreased in animals that were H. pylori-negative at the endoscopy performed at 11.5 months (○; n = 8), whereas it did not change significantly in those who were H. pylori positive at 11.5 months (+ ; n = 18). In animals given placebo plus LT, IgG initially did not change and then increased progressively in the animals that were H. pylori positive at the endoscopy performed at 11.5 months (♦; n = 27). IgG remained low in the two animals that had received placebo plus LT and remained H. pylori negative (data not illustrated). *, P < 0.05 versus placebo plus LT and H. pylori positive at 11.5 months. SE, standard error. (Adapted from reference 36 .)