Esophageal cancer represents a major problem globally, with an estimated 398,000 esophageal squamous cell cancers (ESCC) and 52,000 esophageal adenocarcinomas (EAC) diagnosed worldwide in 2012. The past four decades have witnessed a markedly increasing incidence of oesophageal adenocarcinoma in western regions, including Europe, Northern America and Australia. Male to female incidence ratio of 6-to-1 in general. Risk factors of Adenocarcinoma: diet, obesity (increased intra-abdominal pressure, pro-inflammatory cytokines),smoking, reduction of infection Helicobacter (increased serum levels of Ghrelin), antibiotics (reduction of Helicobacter, increased relative abundance of Firmicutes decreasing Bacteroidetes) The increasing incidence of esophageal adenocarcinoma may be inversely associated with Helicobacter pylori infection (40-60% reduced risk). That is Helicobacter might affect carcinogenesis in the lower esophagus. The prevalence of Helicobacter infection has decreased in Western populations since the middle of the 20th century, which was earlier than the start of the increasing incidence of esophageal cancer.
Differences in bacterial composition of tumour versus normal adjacent tissue included an increased abundance of phylum Firmicutes (85%), and a relative shift of Gram negative to Gram positive microbiota, including saccharolytic Streptococcus. Potential biomarkers of oral squamous cell carcinoma: Prevotella melaninogenica, Capnocytophaga gingivalis and Streptococcus mitis (Sensitivity and specificity ≥ 90%). The type II microbiota is enriched in gram-negative bacteria (more than 50%) and is mainly associated with the abnormal esophagus. These gram-negative bacteria include Veillonella, Prevotella, Haemophilus, Neisseria, Granulicatella and Fusobacterium. Type II microbiome is primarily correlated with reflux esophagitis and Barrett’s esophagus. The type II microbiome produces larger amounts of gram-negative microbial components, such as lipopolysaccharides (LPS), or endotoxin.
In 2009 Yang reported that type I microbiota which is mainly composed of gram-positive bacteria, is closely associated with the normal esophagus and is dominated by the Firmicutes phylum and Streptococcus is the most dominant genus. The type II microbiota is enriched in gram-negative bacteria (more than 50%) and is mainly associated with the abnormal esophagus. These gram-negative bacteria include Veillonella, Prevotella, Haemophilus, Neisseria, Granulicatella and Fusobacterium. Type II microbiome is primarily correlated with reflux esophagitis and Barrett’s esophagus. The type II microbiome produces larger amounts of gram-negative microbial components, such as lipopolysaccharides (LPS), or endotoxin.
The microbial dysbiosis in the esophagus is associated with abnormal esophagus. LPS: lipopolysaccharides; NF-kB nuclear factor kappa; TLRs: toll-like receptors; BE: barrett esophagus; EAC: esophageal adenocarcinoma. The type II microbiome produces larger amounts of gram-negative microbial components, such as lipopolysaccharides (LPS), or endotoxin. Physiological emptying of the stomach after a meal reduces the pressure and reduces the opportunity for reflux. In mice treated with LPS it was found that nearly 80% of food intake remains in the stomach 4 hours after a meal. Cytokines associated with carcinogenesis (IL-18) were more highly expressed in the tissues colonized by Campylobacter species. LPS may stimulate the innate immune system toll-like receptor (TLR) 4 in the epithelial or inflammatory cells, leading to nuclear factor kappa B activation (associated with elevated levels of inflammatory cytokines).
