Damage to the colon mucus barrier, the first line of defense against microorganisms, is an important determinant of intestinal diseases such as inflammatory bowel disease and colorectal cancer, and disorder in extraintestinal organs. The mucus layer has attracted the attention of the scientific community in recent years, and with the discovery of new mucosal components, it has become increasingly clear that the mucosal barrier is a complex system composed of many components. Moreover, certain components are jointly involved in regulating the structure and function of the mucus barrier. Therefore, a comprehensive and systematic understanding of the functional components of the mucus layer is clearly warranted. In this review, we summarize the various functional components of the mucus layer identified thus far and describe their unique roles in shaping mucosal structure and function. Furthermore, we detail the mechanisms underlying mucus secretion, including baseline and stimulated secretion. In our opinion, baseline secretion can be categorized into spontaneous Ca²⁺ oscillation-mediated slow and continuous secretion and stimulated secretion, which is mediated by massive Ca²⁺ influx induced by exogenous stimuli. This review extends the current understanding of the intestinal mucus barrier, with an emphasis on host defense strategies based on fortification of the mucus layer.

Ulcerative colitis (UC) is a chronic recurrent intestinal inflammatory disease characterized by high incidence and young onset age. Recently, there have been some interesting findings in the pathogenesis of UC. The mucus barrier, which is composed of a mucin complex rich in O-glycosylation, not only provides nutrients and habitat for intestinal microbes but also orchestrates the taming of germs. In turn, the gut microbiota modulates the production and secretion of mucins and stratification of the mucus layers. Active bidirectional communication between the microbiota and its ‘slimy’ partner, the mucus barrier, seems to be a continually performed concerto, maintaining homeostasis of the gut ecological microenvironment. Any abnormalities may induce a disorder in the gut community, thereby causing inflammatory damage. Our review mainly focuses on the complicated communication between the mucus barrier and gut microbiome to explore a promising new avenue for UC therapy.

In this paper, nanofibrous membranes based on chitosan (CS), poly (vinyl alcohol) (PVA) and graphene oxide (GO) composites, loaded with antibiotic drugs, such as Ciprofloxacin (Cip) and Ciprofloxacin hydrochloride (CipHcl) were prepared via the electrospinning technique. The uniform and defect-free CS/PVA nanofibers were obtained and GO nanosheets, shaping spindle and spherical, were partially embedded into nanofibers. Besides, the antibiotic drugs were effectively loaded into the nanofibers and part of which were absorbed into GO nanosheets. Intriguingly, the release of the drug absorbed in GO nanosheets regulated the drug release profile trend, avoiding the “burst” release of drug at the release initial stage, and the addition of GO slightly improved the drug release ratio. Nanofibrous membranes showed the significantly enhanced antibacterial activity against Escherichia coli, Staphylococcus aureus and Bacillus subtilis after the addition of antibiotic drug. Moreover, the drug-loaded nanofibrous membranes exhibited excellent cytocompatibility with Melanoma cells, indicative to the great potential potential for applications in wound dressing.

Ulcerative colitis (UC) is an idiopathic, long-term inflammatory disorder of the colon, characterized by a continuous remitting and relapsing course. The intestinal mucus barrier is the first line at the interface between the host and microbiota and acts to protect intestinal epithelial cells from invasion. Data from patients and animal studies have shown that an impaired mucus barrier is closely related to the severity of UC. Depletion of the mucus barrier is not just the strongest but is also the only independent risk factor predicting relapse in patients with UC. Peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear transcription regulator, is involved in the regulation of inflammatory cytokine expression. It is also known to promote mucus secretion under pathological conditions to expel pathogenic bacteria or toxins. More important, PPARγ has been shown to affect host-microbiota interactions by modulating the energy metabolism of colonocytes and the oxygen availability of the intestinal microbiome. It is well known that gut microbiota homeostasis is essential for butyrate generation by the commensal bacteria to supply energy resources for colonocytes. Therefore, it can be speculated that PPARγ, as a central coordinator of the mucus barrier, may be a promising target for the development of effective agents to combat UC.

Sulforaphane (SFN) is a dietary component with multiple bioactivities; however, its role in obesity-related metabolic derangement remains unclear. Here, the effect of SFN on the glucose intolerance of obese mice and the underlying mechanism were determined. C57B/6J male mice were randomly divided into two groups, having free access to water and a normal-fat diet (ND, n = 6) or a high-fat diet (HFD, n = 33) for 8 weeks; thereafter twelve mice having the greatest weight gain among the HFD-fed mice were considered as obese mice. These obese mice were randomly divided into two groups and treated orally for 6 weeks with or without SFN (100 μmol per kg bw, 3 times per week). During this period the animals were continuously maintained on a ND or a HFD. Blood glucose and serum insulin were examined; then glucose tolerance and insulin resistance were evaluated. In addition, the expression of insulin signaling pathway-related genes in the muscle was determined. Our data showed that the obese mice presented a marked insulin resistance and glucose intolerance as compared to the control group, while SFN treatment exerted a prominently protective effect. In addition, the SFN-treated obese mice had a significantly increased insulin receptor substrate 1 (IRS-1) protein level (P < 0.05), markedly elevated Akt activation, as well as dramatically enhanced phosphorylation of PDK-1 (P < 0.05) when compared with the SFN-untreated obese mice. Moreover, the SFN-treated obese mice exhibited a significantly enhanced translocation of GLUT4 (P < 0.05) to the plasma membrane in the muscle compared to the obese mice without SFN treatment. In conclusion, our results support the notion that SFN acts as a promising agent to improve glucose tolerance through the up-regulation of insulin signaling mainly involving the IRS-1/Akt/GLUT4 pathway in the muscle.