The gut microbiota is now considered as one of the key elements contributing to the regulation of host health. Virtually all our body sites are colonised by microbes suggesting different types of crosstalk with our organs. Because of the development of molecular tools and techniques (ie, metagenomic, metabolomic, lipidomic, metatranscriptomic), the complex interactions occurring between the host and the different microorganisms are progressively being deciphered. Nowadays, gut microbiota deviations are linked with many diseases including obesity, type 2 diabetes, hepatic steatosis, intestinal bowel diseases (IBDs) and several types of cancer. Thus, suggesting that various pathways involved in immunity, energy, lipid and glucose metabolism are affected. In this review, specific attention is given to provide a critical evaluation of the current understanding in this field. Numerous molecular mechanisms explaining how gut bacteria might be causally linked with the protection or the onset of diseases are discussed. We examine well-established metabolites (ie, short-chain fatty acids, bile acids, trimethylamine N-oxide) and extend this to more recently identified molecular actors (ie, endocannabinoids, bioactive lipids, phenolic-derived compounds, advanced glycation end products and enterosynes) and their specific receptors such as peroxisome proliferator-activated receptor alpha (PPARα) and gamma (PPARγ), aryl hydrocarbon receptor (AhR), and G protein-coupled receptors (ie, GPR41, GPR43, GPR119, Takeda G protein-coupled receptor 5). Altogether, understanding the complexity and the molecular aspects linking gut microbes to health will help to set the basis for novel therapies that are already being developed.

https://gut.bmj.com/content/gutjnl/71/5/1020.full.pdf

Gut microbiome and health: mechanistic insights

Non-steroidal anti-inflammatory drugs (NSAIDs) and organ damage: A current perspective.

The Healthy Microbiome-What Is the Definition of a Healthy Gut Microbiome?

Nonsteroidal anti-inflammatory drugs (NSAID)s relieve pain, inflammation, and fever by inhibiting the activity of cyclooxygenase isozymes (COX-1 and COX-2). Despite their clinical efficacy, NSAIDs can cause gastrointestinal (GI) and cardiovascular (CV) complications. Moreover, NSAID use is characterized by a remarkable individual variability in the extent of COX isozyme inhibition, therapeutic efficacy, and incidence of adverse effects. The interaction between the gut microbiota and host has emerged as a key player in modulating host physiology, gut microbiota-related disorders, and metabolism of xenobiotics. Indeed, host-gut microbiota dynamic interactions influence NSAID disposition, therapeutic efficacy, and toxicity. The gut microbiota can directly cause chemical modifications of the NSAID or can indirectly influence its absorption or metabolism by regulating host metabolic enzymes or processes, which may have consequences for drug pharmacokinetic and pharmacodynamic properties. NSAID itself can directly impact the composition and function of the gut microbiota or indirectly alter the physiological properties or functions of the host which may, in turn, precipitate in dysbiosis. Thus, the complex interconnectedness between host-gut microbiota and drug may contribute to the variability in NSAID response and ultimately influence the outcome of NSAID therapy. Herein, we review the interplay between host-gut microbiota and NSAID and its consequences for both drug efficacy and toxicity, mainly in the GI tract. In addition, we highlight progress towards microbiota-based intervention to reduce NSAID-induced enteropathy.

/pdf/nsaid-gut-microbiota-interactions-298t43e43i.pdf

NSAID–Gut Microbiota Interactions

Recent advances in small-bowel endoscopy such as capsule endoscopy have shown that non-steroidal anti-inflammatory drugs (NSAIDs) frequently damage the small intestine, with the prevalence rate of mucosal breaks of around 50% in chronic users. A significant proportion of patients with NSAIDs-induced enteropathy are asymptomatic, but some patients develop symptomatic or complicated ulcers that need therapeutic intervention. Both inhibition of prostaglandins due to the inhibition of cyclooxygenases and mitochondrial dysfunction secondary to the topical effect of NSAIDs play a crucial role in the early process of injury. As a result, the intestinal barrier function is impaired, which allows enterobacteria to invade the mucosa. Gram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form. Finally, neutrophils accumulate in the mucosa, resulting in intestinal ulceration. Currently, misoprostol is the only drug that has a proven beneficial effect on bleeding small intestinal ulcers induced by NSAIDs or low-dose aspirin, but its protection is insufficient. Therefore, the efficacy of the combination of misoprostol with other drugs, especially those targeting the innate immune system, should be assessed in the next step.

/pdf/current-knowledge-on-non-steroidal-anti-inflammatory-drug-36xtbws2hx.pdf

Current knowledge on non-steroidal anti-inflammatory drug-induced small-bowel damage: a comprehensive review

Bifidobacterium breve Bif195 Protects Against Small-Intestinal Damage Caused by Acetylsalicylic Acid in Healthy Volunteers

The Gut Microbiota in Causation, Detection, and Treatment of Cancer.

Background and study aims Determining the etiology and location of gastrointestinal motility disorders can be challenging. A range of investigations targeting specific areas of gastrointestinal transit are available, but many provide clinical data for a given gastrointestinal region alone or for non-specific whole gut transit, and are otherwise of limited use. Video capsule endoscopy allows endoscopic visualisation of the entire gastrointestinal tract, and may also provide more specific data for regional transit time abnormalities. Patients and methods Data from video capsules ingested by 71 ambulatory healthy subjects were recorded and analyzed to determine gastric and small bowel transit times in the fasting state. Results Median, and interquartile range (IQR), gastric transit time was 22 (10–48) minutes, and median (IQR) small bowel transit time was 198.5 (157–240.5) minutes. Conclusion These data, for the first time to our knowledge, provide references for gastrointestinal transit times among healthy ambulatory subjects using video capsule endoscopy. This potentially strengthens clinical use of video capsule endoscopy in the investigation of patients with suspected gastrointestinal motility disorders.

/pdf/defining-gastrointestinal-transit-time-using-video-capsule-46oqvnobde.pdf

Defining gastrointestinal transit time using video capsule endoscopy: a study of healthy subjects.

Faecal Microbiota Transplantation (FMT) - classical bedside-to-bench clinical research.

The demand for endoscopic services is increasing rapidly, and this necessitates optimal efficiency in the endoscopy unit. Aim: To assess the efficiency of an endoscopy unit, concentrating in the delay pre-and post-procedure. Patients: Outpatient/day ward procedures. Methods: We examined the delay in endoscopic procedures between 19 and 30 May 2014. The procedure process was examined at three different stages: stage 1 is from when the ‘patients arrives to pre-procedure ward’ to ‘ready for procedure’; stage 2 is from ‘where the patient is ready and waiting to be called’ to ‘when the endoscopy procedure commences’; and stage 3 is from ‘when the ward is contacted to collect patient post procedure’ to ‘when the patient is discharged from the ward’. Results: The pathways for 238 endoscopic procedures were assessed. In total, 249 episodes of delay were documented. Stage 1 accounts for 28% of the delays; there is 1.1–1.6 hours of a delay per patient at this stage. Stage 2 accounts for 53% of the delays; there is ...

Improving efficiency in the endoscopy unit

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