Comparison of gastric body and antral pH: a 24 hour ambulatory study in healthy volunteers.

McLauchlan, G.; Fullarton, G M; Crean, G. P.; McColl, Kenneth E.L.

doi:10.1136/gut.30.5.573

Cited by 91 publications

(69 citation statements)

References 14 publications

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“…Parietal cells also secrete concentrated HCl, which presumably results in more frequent exposure to acid in the corpus. The pH of the corpus, however, is not lower overall than that of the antrum, although it does display a broader range (8,32,51). Thus, the different regions of the stomach possess distinct physiological characteristics that likely present H. pylori with different chemotactic signals.…”

Section: Discussionmentioning

confidence: 97%

Helicobacter pylori Requires TlpD-Driven Chemotaxis To Proliferate in the Antrum

et al. 2012

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ABSTRACTDifferent disease outcomes ofHelicobacter pyloriinfection correlate with distinct inflammation patterns. These different inflammatory distributions may be initiated by differences in bacterial localization. OneH. pyloriproperty known to affect murine stomach localization is chemotaxis, the ability to move in response to chemical cues. In this report, we used nonchemotactic mutants (Che−) to analyze whether chemotaxis is required for initial colonization of particular stomach regions or for subsequent growth therein. We found thatH. pyloribehaves differently in the corpus, antrum, and corpus-antrum transition zone subregions of the stomach. This outcome suggests that these regions contain unique chemotactic signals. In the corpus,H. pyloriutilizes chemotaxis for initial localization but not for subsequent growth. In contrast, in the antrum and the corpus-antrum transition zone, chemotaxis does not help initial colonization but does promote subsequent proliferation. To determine which chemoreceptor is responsible for the corpus-antrum phenotypes, we infected mice with strains lacking each chemoreceptor. Strains lacking TlpA, TlpB, or TlpC displayed only modest deviations from the wild-type phenotype, while strains lacking TlpD resembled the Che−mutant in their antral colonization defect and fared even worse than the Che−mutant in the corpus. Additional analysis showed that inflammation is worse in the antrum than in the corpus in both wild-type and Che−mutant infections. These results suggest that chemotaxis, specifically, that controlled by TlpD, is necessary forH. pylorito survive or grow in the environment of increased inflammation in the antrum.

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Section: Discussionmentioning

confidence: 97%

Helicobacter pylori Requires TlpD-Driven Chemotaxis To Proliferate in the Antrum

et al. 2012

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“…McLauchlan and colleagues (69) reported that pH dynamics after a meal can be more pronounced in the stomach corpus than in the antrum, providing a more challenging environment for H. pylori to colonize persistently (10,11,15). On the other hand, the antrum might provide more inflammation and produce more reactive oxygen than the corpus (25), in particular during late infection.…”

Section: Discussionmentioning

confidence: 99%

Role of Energy Sensor TlpD of Helicobacter pylori in Gerbil Colonization and Genome Analyses after Adaptation in the Gerbil

et al. 2013

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cHelicobacter pylori maintains colonization in its human host using a limited set of taxis sensors. TlpD is a proposed energy taxis sensor of H. pylori and dominant under environmental conditions of low bacterial energy yield. We studied the impact of H. pylori TlpD on colonization in vivo using a gerbil infection model which closely mimics the gastric physiology of humans. A gerbil-adapted H. pylori strain, HP87 P7, showed energy-dependent behavior, while its isogenic tlpD mutant lost it. A TlpD-complemented strain regained the wild-type phenotype. Infection of gerbils with the complemented strain demonstrated that TlpD is important for persistent infection in the antrum and corpus and suggested a role of TlpD in horizontal navigation and persistent corpus colonization. As a part of the full characterization of the model and to gain insight into the genetic basis of H. pylori adaptation to the gerbil, we determined the complete genome sequences of the gerbil-adapted strain HP87 P7, two HP87 P7 tlpD mutants before and after gerbil passage, and the original human isolate, HP87. The integrity of the genome, including that of a functional cag pathogenicity island, was maintained after gerbil adaptation. Genetic and phenotypic differences between the strains were observed. Major differences between the gerbil-adapted strain and the human isolate emerged, including evidence of recent recombination. Passage of the tlpD mutant through the gerbil selected for gain-of-function variation in a fucosyltransferase gene, futC (HP0093). In conclusion, a gerbil-adapted H. pylori strain with a stable genome has helped to establish that TlpD has important functions for persistent colonization in the stomach. Helicobacter pylori chronically colonizes the gastric mucus layer of humans and induces chronic gastritis and, in severe cases, mucosa-associated lymphoid tissue lymphoma or adenocarcinoma of the stomach (1). Motility and chemotaxis are crucial features during the initiation and the persistence of H. pylori colonization, as demonstrated in vivo in mice and Mongolian gerbils (2-8). Chemotaxis allows bacteria to sense environmental stimuli and to navigate toward optimal living conditions. This is particularly important for H. pylori under the harsh conditions of the human stomach. It has been shown that H. pylori loses its motility within minutes in vivo under conditions of low pH and high pepsin activity (9). A proper orientation determined by a combination of stomach conditions/physiology and optimal bacterial tactic abilities is also required for H. pylori to reach its destination during the initial colonization process (10). Indeed, the majority of H. pylori cells detected in vivo in the Mongolian gerbil stomach were located in intimate proximity to the epithelial cells and were guided there by a vertical pH gradient in the stomach mucus (11).In H. pylori, a complete set of chemotaxis genes has been identified, including the established core genes and genes coding for four transducer-like proteins (Tlps), TlpA, TlpB, TlpC, ...

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“…In contrast to the slight alkalinity of the fasting python's stomach, mammals maintain a highly acidic environment (pH 1.1-3) within their stomachs between bouts of digestion (Youngberg et al, 1985;Evans et al, 1988;Cilluffo et al, 1990;Viani et al, 2002). Whereas pythons experience a dramatic postprandial decrease in gastric pH, the luminal pH of mammal stomachs increases rapidly after feeding to range between 3 and 6, presumably as the ingested meal buffers the gastric acid (Savarino et al, 1988;McLauchlan et al, 1989;Cilluffo et al, 1990). Within a few hours after feeding, intragastric pH of mammals drops as acid production, which has increased 20-fold, overwhelms the buffering capacity of the food, which is then being passed through the pyloric sphincter into the small intestine (Fordtran and Walsh, 1973).…”

Section: Gastric Phmentioning

confidence: 99%

Gastric function and its contribution to the postprandial metabolic response of the Burmese pythonPython molurus

Secor

2003

Journal of Experimental Biology

139

141

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SUMMARY The large intact prey ingested by Burmese pythons require considerable processing by the stomach before passage into the small intestine. To investigate the function and cost of gastric digestion and its contribution to postprandial metabolic response for the Burmese python, I examined the rate of gastric digestion, the postprandial profile of gastric pH and the effects of decreasing gastric workload on the metabolic cost of digestion, referred to as specific dynamic action (SDA). Ingested meal mass (equivalent to 25% of snake body mass) was reduced by 18% within 1 day postfeeding, by which time intragastric pH had decreased from 7.5 to 2. Gastric pH was maintained at 1.5 for the next 5–7 days, after which it returned to 7.5. The SDA generated by digesting an intact rat meal was reduced by 9.1%, 26.0%, 56.5% and 66.8%,respectively, when pythons were fed steak, ground rat, liquid diet or ground rat directly infused into the small intestine. The production of HCl and enzymes and other gastric functions represent an estimated 55% of the python's SDA generated from the digestion of an intact rodent meal. Additional contributors to SDA include protein synthesis (estimated 26%),gastrointestinal upregulation (estimated 5%) and the activities of the pancreas, gallbladder, liver, kidneys and intestines during digestion(estimated 14%). Operating on a `pay before pumping' principle, pythons must expend endogenous energy in order to initiate acid production and other digestive processes before ingested nutrients can be absorbed and channeled into metabolic pathways.

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Comparison of gastric body and antral pH: a 24 hour ambulatory study in healthy volunteers.

Cited by 91 publications

References 14 publications

Helicobacter pylori Requires TlpD-Driven Chemotaxis To Proliferate in the Antrum

Helicobacter pylori Requires TlpD-Driven Chemotaxis To Proliferate in the Antrum

Role of Energy Sensor TlpD of Helicobacter pylori in Gerbil Colonization and Genome Analyses after Adaptation in the Gerbil

Gastric function and its contribution to the postprandial metabolic response of the Burmese pythonPython molurus

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