Synthetic chemicals (environmental pollutants, food additives) are widely used for many industrial purposes and consumer-related applications, which implies, through manufactured products, diet, and environment, a repeated exposure of the general population with growing concern regarding health disorders. The gastrointestinal tract is the first physical and biological barrier against these compounds, and thus their first target. Mounting evidence indicates that the gut microbiota represents a major player in the toxicity of environmental pollutants and food additives; however, little is known on the toxicological relevance of the mucus/pollutant interplay, even though mucus is increasingly recognized as essential in gut homeostasis. Here, we aimed at describing how environmental pollutants (heavy metals, pesticides, and other persistent organic pollutants) and food additives (emulsifiers, nanomaterials) might interact with mucus and mucus-related microbial species; that is, “mucophilic” bacteria such as mucus degraders. This review highlights that intestinal mucus, either directly or through its crosstalk with the gut microbiota, is a key, yet underestimated gut player that must be considered for better risk assessment and management of environmental pollution.

The World Health Organization classified processed and red meat consumption as “carcinogenic” and “probably carcinogenic”, respectively, to humans. Haem iron from meat plays a role in the promotion of colorectal cancer in rodent models, in association with enhanced luminal lipoperoxidation and subsequent formation of aldehydes. Here, we investigated the short-term effects of this haem-induced lipoperoxidation on mucosal and luminal gut homeostasis including microbiome in F344 male rats fed with a haem-enriched diet (1.5 μmol/g) 14–21 days. Changes in permeability, inflammation, and genotoxicity observed in the mucosal colonic barrier correlated with luminal haem and lipoperoxidation markers. Trapping of luminal haem-induced aldehydes normalised cellular genotoxicity, permeability, and ROS formation on a colon epithelial cell line. Addition of calcium carbonate (2%) to the haem-enriched diet allowed the luminal haem to be trapped in vivo and counteracted these haem-induced physiological traits. Similar covariations of faecal metabolites and bacterial taxa according to haem-induced lipoperoxidation were identified. This integrated approach provides an overview of haem-induced modulations of the main actors in the colonic barrier. All alterations were closely linked to haem-induced lipoperoxidation, which is associated with red meat-induced colorectal cancer risk.

Introduction: The intestinal barrier controls the absorption of nutrients and water whilst helping to prevent the entry of toxins and pathogenic micro-organisms from the lumen into the tissues. Deficiencies in the barrier are associated with various gastrointestinal and extra digestive disorders. Areas covered: This review provides an overview of the relationship between increased intestinal permeability and disease, and considers the role of mucosal protectants (mucoprotectants) in restoring normal intestinal barrier function, with a particular focus on diarrheal disorders. Expert commentary: Impairment of the intestinal barrier characterizes a variety of diseases, and there is ongoing interest in the development of pharmacological approaches targeting the reduction of intestinal permeability. These include corticosteroids, aminosalicylates and anti-tumor necrosis factor-α (TNF-α), which act by reducing inflammation; probiotics, which modulate the production of mucin and epithelial tight junction proteins; and mucoprotectants, which form a protective film over the epithelium. Recently, preclinical and clinical data highlight, the ability of new mucoprotectants, such as gelatin tannate and xyloglucan, to protect the intestinal mucosa and to exert anti-diarrheal effects. In the future the ability of these substances to enhance the intestinal barrier may extend their use in the management of a variety of gastro-intestinal diseases associated with ‘leaky gut’.

Aim: Reticulated gelatin (RG), hibiscus and propolis (RGHP) is a medical device that can reduce the bacterial adherence to epithelial cultured cells and invasion by enteropathogens, thus gathering relevant properties to decrease the risk of urinary tract infections (UTIs). We aimed at evaluating in Wistar rats the efficacy of RGHP, RG and vehicle against intestinal commensals commonly involved in UTIs. Methods: Animals received orally (with supplemental Na2CO3): RGHP 1540 mg/day/rat; RG 500 mg/day/rat or vehicle. Results: RGHP significantly reduced fecal Escherichia coli and Enterococcus spp. levels without affecting other targeted Enterobacteriaceae. The antagonistic property of RGHP was confirmed in streptomycin-pretreated rats highly colonized with a human commensal E. coli strain with uropathogenic potential. Conclusion: RGHP may decrease the risk of UTIs by reducing colonization by opportunistic uropathogens.

Background: Newer antidiarrheal agents include the mucoprotectants gelatin tannate and xyloglucan. Methods: Rat models of cholera toxin (CT)-induced water secretion were used to evaluate the mucoprotective effects of gelatin tannate, xyloglucan, and related compounds. Results: Oral pretreatment for 4 days with gelatin tannate (250 and 500 mg/kg/day), but not tannic acid or gelatin (both 125 mg/kg/day), blocked CT-induced intestinal water secretion. CT-induced intestinal water secretion was also attenuated by oral xyloglucan 12.5 mg/kg + gelatin 125 mg/kg (6 h pre-CT) and gelatin 250 mg/kg (12 h pre-CT), and by local (intra-jejunal loop) administration of gelatin, gelatin tannate and xyloglucan concomitantly with CT. Conclusions: Gelatin tannate and xyloglucan + gelatin attenuated CT-induced intra-loop water secretion in this experimental model, supporting previous evidence that their mechanisms of mucosal protection are closely related to their chemical structures, which confer film-forming properties via the formation of mucoadhesive films.

Irritable bowel syndrome (IBS) is a functional, gastrointestinal disease characterized by a combination of chronic or recurrent symptoms such as abdominal pain and abnormal bowel habit. Most of the IBS features occur without identifiable organic cause and are strongly influenced by stress and anxiety suggesting the involvement of brain–gut interactions in this disease. Microbiota changes have also been reported such as decreased abundance of the genera Bifidobacterium and Lactobacillus and increased firmicutes: bacteroidetes ratio but there is no consensus on a specific IBS microbiota signature. Psychological stress in rodents impacts intestinal epithelial barrier integrity as well as the composition of microbial communities and induces visceral pain, providing an interesting model for IBS pathophysiology investigation. Modulation of the intestinal microbiota using probiotics in preclinical trials prevents stress-induced visceral hypersensitivity directly through probiotic metabolites production or indirectly through prevention of the intestinal barrier function impairment. The clinical efficacy of probiotic treatments has also been suggested but the use of different scales to analyze the mean differences of symptoms in various studies has limited the ability of all existing meta-analyses in IBS to confirm the effectiveness of probiotics on major IBS symptoms and patient quality of life. Le syndrome de l’intestin irritable (SII), une pathologie fonctionnelle, est caractérisé par une douleur abdominale et des altérations du transit intestinal. Les symptômes du SII ne sont pas associés à une cause organique identifiée, et ils sont impactés par le stress et l’anxiété soulignant l’implication de l’axe intestin–cerveau dans cette pathologie. Des changements du microbiote intestinal ont été aussi observés chez les patients SII vs les sujets sains. Ces changements indiquent une diminution de l’abondance des genres Bifidobacterium et Lactobacillus et une augmentation du ratio Firmicutes/Bacteroidetes. Toutefois, une signature microbienne spécifique du SII n’a pas été établie. Chez l’animal, le stress provoque une augmentation de la perméabilité intestinale, des changements de la composition du microbiote et une hypersensibilité viscérale, suggérant la pertinence de l’utilisation de ce modèle dans l’étude du SII. La modulation du microbiote intestinal par les probiotiques chez l’animal a prévenu l’hypersensibilité viscérale soit directement via des métabolites produits par les probiotiques, soit indirectement en prévenant la rupture de la barrière épithéliale. L’efficacité clinique des traitements probiotiques a été rapportée régulièrement par les méta-analyses, mais la limitation pour confirmer cette efficacité reste associée à l’utilisation d’échelles diverses pour analyser les différences moyennes des symptômes du SII dans les études considérées.