Chronic constipation is a prevalent functional gastrointestinal disorder accompanied with intestinal dysbiosis. However, causal relationship between dysbiosis and constipation remains poorly understood. Serotonin transporter (SERT) is a transmembrane transport protein which re-uptakes excessive 5-hydroxytryptamine (5-HT) from effective location to terminate its physiological effects and involves in regulating gastrointestinal motility. In this study, fecal microbiota from patients with constipation and healthy controls were transplanted into the antibiotic depletion mice model. The mice which received fecal microbiota from patients with constipation presented a reducing in intestinal peristalsis and abnormal defecation parameters including the frequency of pellet expulsion, fecal weight and fecal water content. After fecal microbiota transplantation, the SERT expression in the colonic tissue was significantly upregulated, and the content of 5-HT was decreased which negatively correlated with the gastrointestinal transit time. Moverover, fecal microbiota from the mice which received fecal microbiota from patients with constipation also upregulated SERT in Caco-2 cells. Besides, this process accompanied with the decreased abundance of Clostridium, Lactobacillus, Desulfovibrio, and Methylobacterium and an increased tend of Bacteroides and Akkermansia, which also involved in the impairment of intestinal barrier after FMT. Taken together, intestinal dysbiosis may upregulate the SERT expression and contribute to the development of chronic constipation.

The human gut is inhabited by diverse microorganisms that play crucial roles in health and disease. Gut microbiota dysbiosis is increasingly considered as a vital factor in the etiopathogenesis of irritable bowel syndrome (IBS), which is a common functional gastrointestinal disorder with a high incidence all over the world. However, investigations to date are primarily directed to the bacterial community, and the gut mycobiome, another fundamental part of gut ecosystem, has been underestimated. Intestinal fungi have important effects on maintaining gut homeostasis just as bacterial species. In the present article, we reviewed the potential roles of gut mycobiome in the pathogenesis of IBS and the connections between the fungi and existing mechanisms such as chronic low-grade inflammation, visceral hypersensitivity, and brain-gut interactions. Moreover, possible strategies targeted at the gut mycobiome for managing IBS were also described. This review provides a basis for considering the role of the mycobiome in IBS and offers novel treatment strategies for IBS patients; moreover, it adds new dimensions to researches on microorganism.

A quantitative model of autoregulatory gene expression involving a single gene with time delays and cross-correlated noise sources is investigated. The probability density and mean first passage time (MFPT) of the protein concentration are obtained. The impacts of multiplicative (σ M ) and additive (σ A ) noise intensities, cross-correlation intensity λ between two noises, time delays τ in the degradation process and θ in the synthesis process and time delay β in both processes on the probability density and MFPT of the regime shifts between high and low protein concentration states are discussed, respectively. These results indicate that (i) the regime shifts from a high (or low) protein concentration state to a low (or high) one can be induced by σ M , λ and θ (or σ A and β); (ii) the MFPT as a function of the noise intensity σ M or σ A exhibits one maximum value in the case of λ > 0 or θ > 0, this maximum is a signature of the noise's enhanced stability phenomenon for high protein concentration state; and (iii) τ and β can weaken the stability of high protein concentration state but, in contrast, λ and θ can enhance it in the gene expression dynamics.

LGGs promoted intestinal MUC2 production through regulating S100A10/5-HT4R and the gut microbiota.

No abstract