Gastroesophageal Reflux Disease and Esophageal Cancer

Gastroesophageal Reflux Disease:

The esophageal microbiome mostly initiates from the oropharynx by engulfing or from the upper stomach by gastroesophageal reflux disease (GORD) (Walker and Talley, 2014). The esophageal microbiome are divided in two distinct types: type I is observed in normal esophagus and is conquered by the Streptococcus genus, whereas type II is usually observed in esophagitis and Barrett’s esophagus and it has significant decrease in Gram-positive bacteria and an increase in Gram-negative anaerobic/microaerophilic bacteria (Yang et al., 2009). An experimental study from China on H. pylori -infected mice confirmed that after antibiotic eradication therapy the lower esophageal microbiota was significantly become lesser in number, with further colonization by Staphylococcus, Acinetobacter, and non-spore-forming Bacillus. On the other hand, to the acid rebound theory, the authors hypothesized that the observed microecological changes may persuade lower esophageal sphincter reduction and reflux esophagitis following eradication therapy (Tian et al., 2015). In addition to these findings, a study from Israel assessing gastric fluid bacteria in healthy individuals and patients with Gas- troesophageal Reflux Disease (GERD) (Barrett0s esopha- gus/reflux esophagitis) showed that before and after PPI treatment, esophageal and gastric microbial communities were completely different, mainly presenting an rise in families from the phylum Clostridia in the esophagus (Amir et.al 2014)In order to confirm that the either these microbiome changes are beneficial or harmful for the esophagus needs further study.

 

Esophageal Cancer:

A stable rise in adenocarcinomas of the gastro-esophageal connection and the esophagus has been recognized over the past two decades and is ascribed to GORD, smoking, and alcohol consumption. Conversely, H. pylori may defend against these types of cancers, through gastric atrophy leading to loss of acid, cytokine or hormonal deregulation, and microbiome change (Yang et al., 2009). Two studies over the past year have highlighted the presence of different microbiome forms connected to esophageal cancer (adenocarcinoma and squamous cell carcinoma) and squamous dysplasia. In the first study conducted on healthy Chinese volunteers and patients by means of the Human Oral Microbe Identification Microarray (HOMIM), a significant positive connotation was found between microbial fertility and pepsinogen I/II ratio and an opposite association with esophageal squamous dysplasia (Yu et al., 2014). So, individuals having lower microbial fertility werelikely to have chronic atrophic gastritis and squamous dysplasia. In the second study, directed in the Golestan Province in northern Iran (located in the “esophageal cancer belt”), gastric microbiota from gastric fundal mucosa was estimated in healthy controls and patients with esophageal squamous cell carcinoma (Nasrollahzadeh et al., 2015). A higher profusion of Clostridiales and Erysipelotrichales orders (both belonging to the phylum Firmicutes) was significantly connected with early squamous dysplasia and esophageal squamous cell cancer.

Intestinal Microbiota Alterations:

A study from Germany elaborate the first study of gut microbiota deviations of Mongolian gerbils after 14 months of H. pylori infection. Associated to simple animals and those diseased with mutant strains, chronic infection with H. pylori caused in raised luminal loads of E. coli and Enterococcus spp. in the cecum, along with Bacteroides/Prevotella spp. in the colon. Fur- thermore, Akkermansia, an unproductive species involved in mucus deprivation, was completely abundant in large intestines of H. pylori-infected animals. The authors suggest that H. pylori -persuaded hypochlorhydria and hypergastrinemia might trigger large intestinal microbiota changes, but the precise mechanisms should be further clarified (Heimesaat et al., 2014).

 

References:

  1. Nardone, G., & Compare, D. (2015). The human gastric microbiota: Is it time to rethink the pathogenesis of stomach diseases?. United European gastroenterology journal3(3), 255-260.

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