Relationship between gastric secretion and infection.

Howden, Colin W.; Hunt, R H

doi:10.1136/gut.28.1.96

Cited by 198 publications

(100 citation statements)

References 77 publications

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“…pylori infection might also affect the normal gastrointestinal flora as a result of the reduced gastric acid secretion induced by H. pylori-associated chronic gastritis, contributing to colorectal carcinogenesis (34). Previous studies have indicated that the presence of enteric infection and overgrowth of intestinal bacteria are directly related to a reduction in gastric acid secretion (35)(36)(37). Our previous study demonstrated that CAG-positive asymptomatic middle-aged subjects, as determined by the serum PG levels of PG I ≤70 ng/ml and a PG I/II ratio of ≤3.0, were found to have larger colonic microflora compared to CAG-negative subjects, with an increase in 83% of the genera or groups comprising intestinal microflora (6).…”

Section: Discussionmentioning

confidence: 99%

Elevated risk of recurrent colorectal neoplasia with Helicobacter pylori-associated chronic atrophic gastritis: A follow-up study of patients with endoscopically resected colorectal neoplasia

Inoue

Kato

Yoshimura

et al. 2012

Molecular and Clinical Oncology

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Abstract.In a previous population-based case-control study, we demonstrated an elevated risk of colorectal neoplasia with Helicobacter pylori (H. pylori) infection. The present study investigated the effects of H. pylori-associated chronic gastritis on the development of colorectal neoplasia by analyzing the recurrence of colorectal neoplasia subsequent to endoscopic resection. Ninety-nine patients who had undergone endoscopic resection of colorectal neoplasia were monitored under colonoscopy, and the recurrence of colorectal neoplasia was prospectively investigated. The stage of H. pylori-associated chronic gastritis in each subject was evaluated using a combination of two serum tests: H. pylori antibody and pepsinogen. In the present cohort, colorectal neoplasia recurred at a rate of 15,296/100,000 person-years during the study period. After adjusting for the confounding factors, chronic atrophic gastritis (CAG) was identified as an independent risk factor [adjusted hazard ratio (HR), 2.72; 95% confidence interval, 1.33-5.57], while H. pylori-infected non-atrophic gastritis was not identified as an independent risk factor for recurrent colorectal neoplasia. Colorectal neoplasia recurred earlier and was significantly more frequent in patients with CAG (22,573/100,000 person-years) compared to patients without CAG (11,089/100,000 person-years; P=0.029, log-rank test).Patients with more extensive CAG showed a higher risk of recurrence. These results demonstrated a significant elevation of the risk of recurrent colorectal neoplasia with the establishment and progression of CAG, indicating the involvement of H. pylori infection in the development of colorectal neoplasia. The two serum tests were useful clinical markers for noninvasively evaluating the risk of each individual for recurrent colorectal neoplasia subsequent to endoscopic resection.

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Section: Discussionmentioning

confidence: 99%

Elevated risk of recurrent colorectal neoplasia with Helicobacter pylori-associated chronic atrophic gastritis: A follow-up study of patients with endoscopically resected colorectal neoplasia

Inoue

Kato

Yoshimura

et al. 2012

Molecular and Clinical Oncology

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“…It has been postulated that one of the main functions of gastric acid is to prevent ingested microorganisms from reaching the small intestine, where they have the potential to cause disease or to gain access to other parts of the body (12). Here, we systematically addressed the issue of the effectiveness of gastric acid as an antibacterial barrier by testing the survival of various bacterial pathogens in H ϩ ,K ϩ -ATPase ␤-subunit-deficient and mice with a gastric pH similar to that found in humans.…”

Section: Discussionmentioning

confidence: 99%

“…Iatrogenic hypochlorhydria can be caused by gastric surgery or by drugs that inhibit acid secretion (18). Regardless of the cause, a number of studies have associated hypochlorhydria with an increased risk of infection (12,22). However, as discussed by Martinsen et al (18), gastrointestinal infections themselves reduce gastric acid secretion in humans and animals, and few systematic experimental and epidemiological studies have been performed to determine the contribution of gastric acid to infection resistance.…”

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confidence: 99%

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Influence of Gastric Acid on Susceptibility to Infection with Ingested Bacterial Pathogens

et al. 2008

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Despite the widely held belief that gastric acid serves as a barrier to bacterial pathogens, there are almost no experimental data to support this hypothesis. We have developed a mouse model to quantify the effectiveness of gastric acid in mediating resistance to infection with ingested bacteria. Mice that were constitutively hypochlorhydric due to a mutation in a gastric H ؉ /K ؉ -ATPase (proton pump) gene were infected with Yersinia enterocolitica, Salmonella enterica serovar Typhimurium, Citrobacter rodentium, or Clostridium perfringens cells or spores. Significantly greater numbers of Yersinia, Salmonella, and Citrobacter cells (P < 0.006) and Clostridium spores (P ‫؍‬ 0.02) survived in hypochlorhydric mice, resulting in reduced median infectious doses. Experiments involving intraperitoneal infection or infection of mice treated with antacids indicated that the increased sensitivity of hypochlorhydric mice to infection was entirely due to the absence of stomach acid. Apart from establishing the role of gastric acid in nonspecific immunity to ingested bacterial pathogens, our model provides an excellent system with which to investigate the effects of hypochlorhydria on susceptibility to infection and to evaluate the in vivo susceptibility to gastric acid of orally administered therapies, such as vaccines and probiotics.

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“…In healthy human subjects, inactivation of ingested pathogens is mediated by gastric fluid containing a combination of hydrochloric acid and proteolytic enzymes (Tennant et al, 2008). Correspondingly, impaired gastric acid secretion is associated with an increased risk of infection (Howden and Hunt, 1987). Hypochlorhydria can result from atrophic gastritis, gastric surgery or drugs that inhibit acid secretion (Martinsen et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Immune status, antibiotic medication and pH are associated with changes in the stomach fluid microbiota

et al. 2013

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The stomach acts as a barrier to ingested microbes, thereby influencing the microbial ecology of the entire gastrointestinal (GI) tract. The stomach microbiota and the role of human host and environmental factors, such as health status or medications, in shaping its composition remain largely unknown. We sought to characterize the bacterial and fungal microbiota in the stomach fluid in order to gain insights into the role of the stomach in GI homeostasis. Gastric fluid was collected from 25 patients undergoing clinically indicated upper endoscopy. DNA isolates were used for PCR amplification of bacterial 16S ribosomal RNA (rRNA) genes and fungal internal transcribed spacers (ITS). RNA isolates were used for 16S rRNA cDNA generation and subsequent PCR amplification. While all stomach fluid samples are dominated by the phyla Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria and Fusobacteria (499% of sequence reads), the transcriptionally active microbiota shows significant reduction in Actinobacteria (34%) and increase in Campylobacter (444%) (Po0.003), specifically the oral commensal and suspected intestinal pathogen Campylobacter concisus. Bacterial but not fungal diversity is reduced by antibiotic treatment (28%; Po0.02), immunosuppression in transplant recipients and HIV/AIDS patients (42%; Po0.001) and gastric fluid pH 44 (70%; Po0.05). Immunosuppression correlates with decreased abundance of Prevotella (24%), Fusobacterium (2%) and Leptotrichia (6%) and increased abundance of Lactobacillus (3844%) (Po0.003). We have generated the first in-depth characterization of the human gastric fluid microbiota, using bacterial 16S rRNA gene and transcript, and fungal ITS amplicon sequencing and provide evidence for a significant impact of the host immune status on its composition with likely consequences for human health.

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Relationship between gastric secretion and infection.

Cited by 198 publications

References 77 publications

Elevated risk of recurrent colorectal neoplasia with Helicobacter pylori-associated chronic atrophic gastritis: A follow-up study of patients with endoscopically resected colorectal neoplasia

Elevated risk of recurrent colorectal neoplasia with Helicobacter pylori-associated chronic atrophic gastritis: A follow-up study of patients with endoscopically resected colorectal neoplasia

Influence of Gastric Acid on Susceptibility to Infection with Ingested Bacterial Pathogens

Immune status, antibiotic medication and pH are associated with changes in the stomach fluid microbiota

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