In jejunal enteral nutrition cases, gastrointestinal symptoms might be caused, for example intractable diarrhea, dumping syndrome. Therefore in the guidelines for jejunal enteral nutrition, it is recommended that liquid nutrients should be dripped slowly to prevent those symptoms. However, limitation for volume of nutrients, and time constraints due to long time dripping will be an issue. For those reasons, jejunal enteral nutrition causes much stress to both patients and caregivers and lowers quality of life. In jejunal feeding cases by percutaneous trans-esophageal gastro-tubing (PTEG), the semi-solidification technique using pectin solution will be the key. This technique reacts free calcium ions in the liquid nutrients with pectin to increase the viscosity of the nutrients and slow down the progress of the nutrients in the gastrointestinal tract. It has made it possible to administer nutrients in a short time without causing those gastrointestinal symptoms. Because this technique can be used not only for PTEG, but also is useful for other enteral nutrition through a thin and long tube, for example naso-gastric tubing (NGT), PEG-jejunal tubing (PEG-J), JET-PEG, we report its efficacies.

The incidence of inflammatory bowel disease (IBD) is increasing worldwide, suggesting a potential role of western diets. Western diet is abundant in dietary fructose, suggesting involvement with the rising incidence of IBD. High fructose diet (HFrD) is reported to exacerbate dextran sodium sulfate (DSS) induced colitis. Additionally, chronic colitis induced by IBD is a risk factor of colitic cancer, which may be exacerbated by HFrD-induced colitis. Furthermore, expression levels of glucose transporter 5 (GLUT5) is downregulated in IBD patients with severe ileitis, which may exacerbate HFrD-induced colitis through fructose influx to the colon. In this review article, we introduce that HFrD 1. worsens experimental colitis in a microbiota-dependent manner, 2. worsens chronic colitis and induces colitis-associated tumorigenesis, which is prevented by dietary interventions, 3. worsens experimental colitis in GLUT5 knockout mouse models mediated through the gut microbiota.

Inflammatory bowel disease refers to two main diseases: ulcerative colitis and Crohn's disease. The number of patients with both diseases in Japan has been increasing rapidly in recent years. Infliximab, an anti-TNF-α antibody, showed dramatic efficacy against inflammatory bowel disease, leading to a paradigm shift in the treatment strategy for inflammatory bowel disease. Since infliximab, drug development for inflammatory bowel disease has completely shifted to molecular targeted therapies. Although the cause of inflammatory bowel disease is unknown, it is hypothesized that environmental factors such as diet, in addition to genetic background, cause dysbiosis of the gut microbiota, which in turn abnormally activates the intestinal immune system and induces chronic inflammation in the gut. Fecal microbiota transplantation (FMT) has attracted attention as an attempt to correct dysbiosis and treat inflammatory bowel disease. Several randomized controlled trials have demonstrated the efficacy of FMT for ulcerative colitis. However, optimization of the administration method, donor selection, and frequency of administration is needed. Long-term outcomes and safety must also be verified.

Dietary fiber in diet is primarily metabolized by human gut bacteria. Lipopolysaccharide (LPS) is an outer membrane component of the bacteria, which may regulate inflammation in the host human body. This study was designed to investigate how the biosynthesis of LPS in the gut microbiota varies with the balance of nutrients in the diet, especially to examine the relationship between the proportion of dietary fiber intake and LPS biosynthesis of gut microbiota. This study was conducted on 927 disease-free participants who gave informed consent in writing or on the web. The proportion of dietary fiber intake was calculated as the relative proportion of dietary fiber intake to the sum of protein, fat, carbohydrate, and dietary fiber intake (energy equivalent) in diet based on the Food Frequency Questionnaire. The biosynthesis of LPS was predicted by meta-16S rRNA gene analysis and PICRUSt2 as the relative proportion of LPS biosynthetic pathways present in the gut microbiota. The proportion of the LPS biosynthetic pathway was higher in obese than in normal-weight participants. Furthermore, the proportion of the LPS biosynthetic pathway was shown to be significantly associated with the proportion of dietary fiber intake, although not with that of protein, fat, or carbohydrate intake. However, in the participants by body mass index (BMI) category (lean, normal-weight, obese), a significant decrease in the proportion of LPS biosynthesis pathway due to the proportion of dietary fiber intake was detected only in the normal-weight group. These results suggest that the proportion of dietary fiber intake is associated with the biosynthesis of LPS of the gut microbiota, and also suggest the possibility that the effect of dietary fiber intake on the LPS depends on the host human's BMI.

Atopic dermatitis (AD) is characterized by pruritus and eczema and is caused by biased differentiation of type 2 helper T cells (Th2). Regulatory T cells (Treg) regulate the immune response and prevent the development of AD. Because AD is closely associated with the gut microbiota, we focused on the probiotic Bifidobacterium breve strain Yakult (BY) . In this study, we investigated the effect of oral administration of BY on AD in Nc/Nga mice. Picryl chloride solution was applied onto the backs of the mice to induce AD. We then orally administered tap water (0.2 mL/day) to mice in the AD group and BY solution (5×10⁹ CFU/0.2 mL/day) to mice in the BY group. The control group comprised mice in which AD was not induced; these mice were orally administered tap water (0.2 mL/day). After the experimental period, the skin on the back and small intestinal specimens were collected from the mice and examined. The lesions on the back showed greater improvement in the BY group than in the AD group. The expression level of cyclooxygenase-2 was significantly decreased in the lesion site. Th1 and Th2 expression levels were lower and Treg expression levels were higher in the BY group than in the AD group. In the small intestine, the Th1 and Treg expression levels were higher and the Th2 expression levels were lower in the BY group than in the AD group. In the lesion site, BY treatment improved AD by suppressing Th2 expression levels with an increase in Treg expression levels. In the small intestine, the increase in Treg expression levels also improved the immune balance. These results suggest that administration of BY improves AD through improvement of intestinal immunity.

Abnormal immune response and disturbance of intestinal microbiome have been reported as the onset factors of atopic dermatitis (AD). Apple pectin has been reported to selectively stimulate proliferation of specific intestinal bacteria and to lower histamine levels in the blood, so it is expected to have preventive effects against allergic diseases. However, its efficacy in improving AD has not been clarified. In this study, we investigated the ameliorating effect of apple pectin on AD and its effect on microbiome.

To induce AD, a picryl chloride solution was applied to shaved back skin of male NC/Nga mice. Treatment groups of AD mice then received oral administration of an apple pectin solution (0.4％ or 4％) for 35 days.

Compared with untreated AD mice, both apple pectin-treated groups showed improvement in skin symptoms of AD. Apple pectin treatment reduced the expression of COX-2, as well as TSLP and IL-4 (p < 0.05). Additionally, increased expression of IFN-γ and Foxp3 were observed in the apple pectin-treated groups (p < 0.05). Regarding intestinal bacteria, the 4％ pectin group showed a tendency toward lower Firmicutes and a tendency toward higher Bacteroidetes compared to the AD group (p = 0.103).

Our findings suggest that ingestion of apple pectin impacted AD by improving the Th1/Th2 balance at the site of AD onset, suppressing skin inflammation, and changing composition of intestinal microbiome in the AD mouse model.

Atopic dermatitis (AD) is a chronic skin disease characterized by itchy eczema that repeatedly worsens and goes into remission. Recently, it has been suggested that there is a close relationship between the inflammation and symptom progression of atopic dermatitis and the intestinal microbiota. This is based on reports that the intestinal microbiota is biased in AD patients and that administration of probiotics is effective in the prevention and treatment of AD. In this study, Lactiplantibacillus plantarum FKW200108 (LB), a lactic acid bacterium derived from funazushi, a specialty of Shiga Prefecture, where the number of patients with allergic diseases is small, was orally administered to AD model mice to investigate its effectiveness in improving symptoms.

Method: NC/Nga mice (approx. 30g/male), a human model of AD, were used. The control group was reared normally, the AD group was induced by using picryl chloride on the back, and the LB group was induced by orally administering LB suspension. After 35 days of rearing, skin samples from the back and small intestine were collected for examination.

Results: In the back skin of mice, the LB group showed improved damage compared to the AD group. In addition, COX-2 protein expression levels were significantly decreased in the LB group compared to the AD group in the back skin (p < 0.05). IFN-γ mRNA expression levels were significantly decreased in the LB group compared to the AD group in the back skin (p < 0.05) and increased in the LB group compared to the AD group in the small intestine (p = 0.09). In addition, IL-4 mRNA expression levels were significantly decreased in the LB group compared to the AD group in the back skin and small intestine (p < 0.05). In addition, FOXP3 mRNA expression levels tended to decrease in the LB group compared to the AD group in the back skin and small intestine (p = 0.15, p = 0.17).

Discussion: It was suggested that administration of LB suspension improves AD symptoms by improving the composition of the intestinal microflora and adjusting the immune balance.