Effects of cagA+ and cagA– strains of Helicobacter pylori on the human gastric mucus layer thickness

Al-Marhoon, Mohammed S.; Nunn, Sheila; Soames, Roger

doi:10.1111/j.1440-1746.2005.03853.x

Cited by 7 publications

(7 citation statements)

References 27 publications

(36 reference statements)

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“…In a study by Lindahl et al, characterizing aspirated gastric fluids from healthy volunteers, no genderrelated differences in electrolyte concentrations, osmolality, bile salt concentrations and protein content between men and women were observed (Lindahl et al, 1997). Furthermore, Al-Marhoon et al reported similar mean mucus layer thickness when comparing men to women (55.5 ± 1.1 vs. 48.2 ± 1.1 µm, respectively) (Al-Marhoon et al, 2005). Although literature reports on gender-related differences remain scarce, this study suggests that gender most likely does not influence mucus layer thickness.…”

Section: Gender and Racesupporting

confidence: 53%

“…Although no age-related changes in mucus layer thickness were observed in H. pylori negative subjects, mucus layer thickness was found to significantly decrease with age in H. pylori positive subjects (Newton et al, 2000). Again, it may be hypothesized that this change might be due to a higher prevalence of gastric atrophy and gastritis in elderly subjects as a result of long-time infection with H. pylori (Al-Marhoon et al, 2005;Newton et al, 2000). Lastly, Feldman et al investigated changes in basal and peak pepsin output (BPO/PPO) in relation to age.…”

Section: Ageelderlymentioning

confidence: 86%

“…Part of this mucus layer is in close contact with the gastric mucosa, while a second part is loosely associated with the former part of the mucus layer and responsible for the lubrication of gastric contents (Allen and Flemstrom, 2005;Cone, 2009). Mucus layer thickness (mean thickness: 50 -200 µm, Table 1) is susceptible to constant changes as it depends on the interplay between layer erosion/degradation and mucus secretion (Al-Marhoon et al, 2005;Cone, 2009;Jordan et al, 1998;Newton et al, 1998;Newton et al, 2000). The presence of mucins in gastric fluids results in shear-thinning behaviour of most gastric aspirates.…”

Section: Viscosity Of Gastric Fluidsmentioning

confidence: 99%

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The dynamic gastric environment and its impact on drug and formulation behaviour

Abeele

Rubbens

Brouwers

et al. 2017

European Journal of Pharmaceutical Sciences

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Section: Gender and Racesupporting

confidence: 53%

Section: Ageelderlymentioning

confidence: 86%

Section: Viscosity Of Gastric Fluidsmentioning

confidence: 99%

See 1 more Smart Citation

The dynamic gastric environment and its impact on drug and formulation behaviour

Abeele

Rubbens

Brouwers

et al. 2017

European Journal of Pharmaceutical Sciences

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“…Furthermore, the expression patterns of gastric mucins MUC5AC and MUC6 seem to be altered in H. pylori-infected patients and skewed toward more MUC6 (5,37). Measurements of mucus thickness in biopsies have shown both a decreased mucus thickness in H. pylori-positive subjects (27,31) as well as no difference in mucus thickness between H. pylori-positive and -negative subjects (1,2,24,25). The present study is the only study presenting mucus thickness values from in vivo measurements including the accumulation rate.…”

Section: Discussionmentioning

confidence: 99%

Impaired mucus-bicarbonate barrier inHelicobacter pylori-infected mice

Henriksnäs

Phillipson²,

Storm³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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To resist the harsh intrinsic milieu, several lines of defense exist in the stomach. The aim of this study was to investigate the effect of the gastric pathogen Helicobacter pylori on these mechanisms in vivo. We used FVB/N mice expressing human ␣-1,3/4-fucosyl transferase (producing Lewis b epitopes) and inoculated with H. pylori 1. Mice were anesthetized with isoflurane or Hypnorm-midazolam, the stomach was exteriorized, and the surface of the corpus mucosa was exposed. Mucus thickness was measured with micropipettes, juxtamucosal pH (pHjm) was measured with pH-sensitive microelectrodes, blood flow was measured with laser-Doppler flowmetry, and mRNA levels of the bicarbonate transporter SLC26A9 were quantified with real-time PCR. The increase in mucosal blood flow seen in response to luminal acid (pH 1.5) in control animals (140 Ϯ 9% of control) was abolished in infected mice. The firmly adherent mucus layer was significantly thinner in infected mice (31 Ϯ 2 m) than in control mice (46 Ϯ 5 m), and no mucus accumulation occurred in infected mice. pHjm decreased significantly more on exposure to luminal acid in infected mice (luminal pH 1.5, pH jm 2.4 Ϯ 0.7) than in control mice (pHjm 6.4 Ϯ 0.5). Despite reduced pHjm, SLC26A9 mRNA expression was significantly, by increased 1.9-fold, in infected mice. The reduction in pH jm by infection with H. pylori might be due to a reduced firmly adherent mucus layer, increased mucus permeability to H ϩ , and/or inhibition of bicarbonate transport. The upregulation of SLC26A9 in H. pylori-infected epithelium might be a result of continuous inhibition of the transporter, e.g., by ammonium, a H. pylori product, which has been previously shown to inhibit SLC26A9. juxtamucosal pH; blood flow; laser-Doppler flowmetry; permeability

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“…Once adhering to the gastric mucosa the bacteria can freely divide, so that within 3 days they cover the gastric epithelial surface and penetrate the gastric glands. Most interesting is the extreme thickness of the mucus layer, which is normally approximately 50–170 µ thick [23], i.e. 10–20 epithelial cell depths.…”

Section: Unique Relationship Between H Pylori and The Gastric Mucosamentioning

confidence: 99%

Helicobacter pylori as a Vaccine Delivery System

Marshall

Schoep

2007

Helicobacter

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For more than 10 years a vaccine against Helicobacter pylori has been the elusive goal of many investigators. The need for a vaccine was highlighted when eradication attempts in developing countries were foiled by reinfection rates of 15-30% per annum. In addition, physicians in developed countries were concerned that attempts at total eradication of H. pylori would result in widespread macrolide resistance in both H. pylori and other important pathogens. Although attempts to produce vaccines against H. pylori have failed in their ultimate goal, considerable knowledge has been developed on the pathogenesis and immunology of Helicobacter infections. In this article we describe an alternative use for this new knowledge, i.e. a plan to use live Helicobacter species to deliver vaccines against other organisms. Because of its intimate attachment to the gastric mucosa and long-term residence there, H. pylori might succeed as an antigen delivery system, a goal which has eluded most other strategies of nonparenteral vaccination.

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Effects of cagA+ and cagA– strains of Helicobacter pylori on the human gastric mucus layer thickness

Abstract: The human gastric mucus thickness is not affected by infection with cagA+ or cagA- strains of H. pylori compared with uninfected. Although a trend of increased mucus thickness with cagA+ infection was observed.

Cited by 7 publications

References 27 publications

The dynamic gastric environment and its impact on drug and formulation behaviour

The dynamic gastric environment and its impact on drug and formulation behaviour

Impaired mucus-bicarbonate barrier inHelicobacter pylori-infected mice

Helicobacter pylori as a Vaccine Delivery System

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