Cigarette smoking is a known risk factor in a number of gastrointestinal (GI) diseases in which the microbiota is implicated, including duodenal ulcer and Crohn’s disease. Smoking has the potential to alter the microbiota; however, to date, the impact of smoking on the mucosa-associated microbiota (MAM), and particularly that of the upper GI tract, remains very poorly characterised. Thus, we investigated the impact of smoking on the upper small intestinal MAM. A total of 102 patients undergoing upper GI endoscopy for the assessment of GI symptoms, iron deficiency, or Crohn’s disease, but without identifiable lesions in the duodenum, were recruited. Smoking status was determined during clinical assessment and patients classified as current (n = 21), previous smokers (n = 40), or having never smoked (n = 41). The duodenal (D2) MAM was profiled via 16S rRNA gene amplicon sequencing. Smoking, both current and previous, is associated with significantly reduced bacterial diversity in the upper small intestinal mucosa, as compared to patients who had never smoked. This was accompanied by higher relative abundance of Firmicutes, specifically Streptococcus and Veillonella spp. The relative abundance of the genus Rothia was also observed to be greater in current smokers; while in contrast, levels of Prevotella and Neisseria were lower. The MAM profiles and diversity of previous smokers were observed to be intermediate between current and never smokers. Smoking did not impact the total density of bacteria present on the mucosa. These data indicate the duodenal MAM of current smokers is characterised by reduced bacterial diversity, which is partially but not completely restored in previous smokers. While the precise mechanisms remain to be elucidated, these microbiota changes may in some part explain the adverse effects of smoking on mucosa-associated diseases of the GI tract. Smoking status requires consideration when interpreting MAM data.

Summary: Background: Study of the upper gastrointestinal microbiome has shown that other bacteria besides Helicobacter pylori flourish despite the hostile environment. Whilst H. pylori is the most studied bacteria in this region with a defined role in inflammation and neoplasia, it is apparent that other bacteria may contribute to UGI disease.Aim: To review current knowledge of bacteria inhabiting the oesophagus, stomach and duodenum.Methods: Published studies on the upper gastrointestinal microbiome (extracted from PubMed during the last 20 years).Results: The stomach is a hostile environment for bacteria; however, recent studies categorising the microbiota have shown surprising results. Helicobacter pylori has been intensively studied since 1984 and recent sequencing analysis of other gastric microbiota shows that H. pylori is not alone. Composition can be influenced by acid suppression, gastritis and abundance of H. pylori. Eradication of H. pylori, whilst decreasing gastric cancer is associated with an increase in asthma, reflux and obesity. A future approach may be to selectively eradicate bacteria which predispose to inflammation and cancer as opposed to a comprehensive knockout policy. In the oesophagus, viridans streptococci are the most common bacteria influenced by both oral and gastric bacteria. Oesophagitis and Barrett's oesophagus are characterised by a significant decrease in Gram‐positive bacteria and an increase in Gram‐negative bacteria. An inverse association of H. pylori and oesophageal adenocarcinoma is described. The duodenal microbiome has been shown to influence small intestinal bacterial overgrowth, irritable bowel syndrome and coeliac disease. The numbers of bacteria recoverable by culture are variable in the stomach mucosa and gastric juice, typically 10²–10⁴ colony‐forming units (CFU)/g or mL and in the oesophagus, up to 10⁴ bacteria per mm² mucosal surface. In the small bowel, in health, 10³ CFU/mL are normal.Conclusion: This review highlights current knowledge of upper gastrointestinal bacteria and associations with disease.

Summary: Background: Current data on small intestinal bacterial overgrowth (SIBO) in patients with inflammatory bowel diseases (IBD) are controversial.Aim: To conduct a systematic review and meta‐analysis to determine the prevalence of SIBO in patients with ulcerative colitis (UC) and Crohn's disease (CD).Methods: Electronic databases were searched up to May 2018 for studies reporting prevalence of SIBO in IBD patients. The prevalence rate of SIBO among IBD patients and the odds ratio (OR) and 95% CI of SIBO in IBD patients compared with controls were calculated.Results: The final dataset included 11 studies (1175 adult patients with IBD and 407 controls), all utilising breath test for diagnosis of SIBO. The proportion of SIBO in IBD patients was 22.3% (95% CI 19.92‐24.68). The OR for SIBO in IBD patients was 9.51 (95% CI 3.39‐26.68) compared to non‐IBD controls, and high in both CD (OR = 10.86; 95% CI 2.76‐42.69) and UC (OR = 7.96; 95% CI 1.66‐38.35). In patients with CD, subgroup analysis showed the presence of fibrostenosing disease (OR = 7.47; 95% CI 2.51‐22.20) and prior bowel surgery (OR = 2.38; 95% CI 1.65‐3.44), especially resection of the ileocecal valve, increased the odds of SIBO. Individual studies suggest that combined small and large bowel disease but not disease activity may be associated with SIBO.Conclusions: Overall, there is a substantial increase in the prevalence of SIBO in IBD patients compared to controls. Prior surgery and the presence of fibrostenosing disease are risk factors for SIBO in IBD.

Summary: Background: The pathogenesis of functional GI disorders (FGIDs) is uncertain. However, underlying immune activation and psychological distress has been documented in irritable bowel syndrome (IBS) and functional dyspepsia (FD). Epidemiological data from the UK suggest that FGIDs are linked to atopy and certain autoimmune diseases but this has not been confirmed.Aim: To test if allergic or autoimmune diseases are independently associated with FGIDs, irrespective of psychological distress in a large population based study.Methods: A total of 3542 people (mean age 57.9 years and 52.7% females) randomly selected from the Australian population, returned a mail survey (response rate = 43%). The survey asked about a physician diagnosis of autoimmune disease (scleroderma, psoriasis, rheumatoid arthritis and diabetes mellitus) or allergic conditions (asthma, food, pollen and/or animal allergy). The questionnaire assessed psychological distress and Rome III criteria for FD and IBS.Results: Asthma, food, pollen and animal allergies, psoriasis and rheumatoid arthritis were univariately significantly associated with IBS and FD. Food allergy (OR = 1.66; 95% CI = 1.15‐2.40, P = 0.007), psoriasis (OR = 1.81; 95% CI = 1.19‐2.74, P = 0.006) and rheumatoid arthritis (OR = 1.68; 95% CI = 1.15‐2.4, P = 0.007) were independent risk factors for IBS, controlling for age, gender and psychological distress. In FD, asthma (OR = 1.32; 95% CI = 1.04‐1.68, P = 0.025) and food allergy (OR = 1.78; 95% CI = 1.28‐2.49, P = 0.001) were independent predictors, controlling for age, sex and psychological distress.Conclusions: There is evidence that both atopic and autoimmune diseases are risk factors for FGIDs, independent of psychological distress, differing in IBS and FD. This provides evidence that different peripheral pathways may be involved in the pathogenesis of certain FGIDs.