Efficacy of sequential fecal-marker examination for evaluating gastrointestinal inflammation in solid food protein-induced enterocolitis syndrome.

BACKGROUND: Food protein-induced enterocolitis syndrome caused by solid foods (Solid-FPIES) is a non-immunoglobulin E-mediated allergic disease characterized by delayed gastrointestinal symptoms. An oral food challenge (OFC) test, although necessary, can be inconclusive in cases with mild symptoms. Moreover, limited diagnostic marker availability highlights the need for novel surrogate markers. We aimed to examine the efficacy of fecal hemoglobin (FHb), lactoferrin (FLf), and calprotectin (FCp) over time in evaluating gastrointestinal inflammation degree in Solid-FPIES. METHODS: This observational study included 40 patients and 42 episodes at Juntendo University Hospital and affiliated hospitals between October 2020 and March 2024 categorized into FPIES (12 patients with 11 egg yolk, 1 fish, and 1 soybean episodes), control (14 patients with 15 episodes), and remission (14 patients). Fecal tests were performed for 7 days following antigen exposure. The ratios of each value were divided by the baseline value and analyzed over time course. RESULTS: The FPIES group had significantly higher peak ratios of all fecal markers than the control group (p < 0.01). The median FHb, FLf, and FCp ratios were 3.25, 9.09, and 9.79 in the FPIES group and 1.08, 1.29, and 1.49 in the control group, respectively. In the remission group, several patients had fluctuating fecal markers despite negative OFC, and one patient was diagnosed with FPIES by OFC with increased load. Receiver operating characteristic curve analyses revealed high diagnostic performance for each fecal marker in FPIES. CONCLUSIONS: Sequential fecal marker examination proved valuable in diagnosing Solid-FPIES and evaluating the degree of gastrointestinal inflammation.

Evaluating Small Intestinal Motility in a Rat Model of Adolescent Irritable Bowel Syndrome.

Objectives: The correlation between altered small intestinal motility and irritable bowel syndrome is not well evaluated. This study aimed to assess the small intestinal and colonic transits in an adolescent irritable bowel syndrome rat model with restraint stress and determine the role of small intestinal motility in the irritable bowel syndrome pathophysiology. Materials: Restraint stress was utilized to prepare adolescent irritable bowel syndrome rat models that were evaluated for clinical signs, including stool frequency and diarrhea. The small intestinal motility and transit rate were also evaluated. Methods: The amounts of mRNA encoding corticotropin-releasing hormone, mast cell, and serotonin (5-Hydroxytryptamine) receptor 3a were quantified using real-time polymerase chain reaction; the 5-Hydroxytryptamine expression was evaluated using immunostaining. Results: Restraint stress significantly increased the number of fecal pellet outputs, stool water content, and small intestinal motility in the adolescent irritable bowel syndrome rat models. There was no difference in real-time polymerase chain reaction results; however, immunostaining analysis revealed that 5-Hydroxytryptamine expression in the small intestine was significantly increased in the adolescent irritable bowel syndrome rat models. Conclusions: In the rat model of adolescent irritable bowel syndrome with restraint stress, we observed an increase in small intestinal and colonic motility. In the small intestine, enhanced 5-Hydroxytryptamine secretion in the distal portion may be involved in increasing the small intestinal motility. Although the present study focused on 5-Hydroxytryptamine, further investigation of other factors that regulate intestinal peristalsis may lead to the establishment of more effective treatment methods for adolescent irritable bowel syndrome.

Breast-feeding regulates immune system development via transforming growth factor-ß in mice pups.

BACKGROUND: Breast milk contains important nutrients and immunoregulatory factors that are essential for newborn infants. Recently, epidemiological studies suggested that breast-feeding prevents a wide range of infectious diseases and lowers the incidence of infant allergic diseases. METHODS: To examine the effects of breast milk on immunological development in infancy, we established an artificial rearing system for hand-feeding mice and compared mouse pups fed with either breast milk or milk substitute. All mice were killed at 14 days of age and immune cells in the thymus, spleen, and small intestine were examined on flow cytometry. RESULTS: The number of thymocytes was higher whereas that of total immune cells of peripheral lymphoid tissues was lower in mice fed breast milk compared with milk substitute-fed mice. In peripheral lymphoid tissues, the proportion of B cells was higher and that of CD8+ T cells, macrophages, dendritic cells, and granulocytes was significantly lower in breast milk-fed mice. The same alteration in immune cells of the thymus and peripheral lymphoid tissues in milk substitute-fed mice was also observed in pups reared by mother mice treated with anti-transforming growth factor-ß (anti-TGF-ß) monoclonal antibody. CONCLUSIONS: Breast milk regulates the differentiation and expansion of innate and adaptive immune cells partly due to TGF-ß. Hence, TGF-ß in breast milk may be a new therapeutic target for innate immune system-mediated diseases of infancy.