Ingestion of paddy rice increases intestinal mucin secretion and goblet cell number and prevents dextran sodium sulfate-induced intestinal barrier defect in chickens

Abstract

Paddy rice is a potential feed grain for chickens, whose strong gizzards can crush the hull. Here, we investigated whether paddy rice rich in hull-derived water-insoluble dietary fiber stimulates intestinal mucin secretion and production, as well as the possible involvement of paddy rice in intestinal barrier function. Layer male chicks at 7 d of age were divided into four groups according to the diet: corn, polished rice, brown rice, or paddy rice (650 g/kg diet), which they ate for 14 consecutive days. At 21 d of age, the birds were refed their experimental diets, and small intestinal mucin fractions were collected to determine intestinal mucin content. Small intestinal mucin secretion was induced most strongly in the paddy rice group (Experiment 1). The rank order of diet-induced mucin secretion was paddy rice > corn = brown rice > polished rice. Ileal MUC2 gene expression and ileal number of goblet cells were highest in the paddy rice group (Experiment 1). A study of bromodeoxy-U uptake into ileal epithelial cells indicated the increase in goblet cells in the paddy rice group was related to accelerate epithelial cell migration (Experiment 2). A single supplementation of isolated rice hulls without kernels increased MUC2 gene expression and goblet cell numbers (Experiment 3), suggesting the importance of the hull's bulk-forming capacity on mucin production. Finally, chicks fed corn or paddy rice were orally administered dextran sodium sulfate (DSS) to disrupt intestinal barrier function. In the DSS-treated birds, the intestinal permeability of fluorescein isothiocyanate dextran in the everted gut sacs was much lower in the paddy rice group than in the corn group (Experiment 4), showing that paddy rice protects against mucosal disruption. In conclusion, ingestion of paddy rice increases intestinal mucin secretion and production through enhanced MUC2 gene expression and epithelial turnover and prevents DSS-induced intestinal barrier defects in chickens.

Effects of Spirogyra jaoensis as a dietary supplement on growth, pectoralis muscle performance, and small intestine morphology of broiler chickens

“…The results of our research showed that administration of S. jaoensis increased the number and area of goblet cells (Table-4), suggesting that mucin production in the small intestine is higher in the treatment groups. Elevated intestinal mucin along with higher epithelial turnover may increase the effectiveness of the small intestine in nutrient absorption [42].…”

<i>Lactobacillus reuteri</i> Enhances the Mucosal Barrier Function against Heat-killed <i>Salmonella</i> Typhimurium in the Intestine of Broiler Chicks

“…Permeability in the ileum and cecum was examined using fluorescein isothiocyanate (FITC) -labeled dextran with a molecular weight of 4,000 (FD-4, Sigma Aldrich, St Louis MO, USA) and a modified version of the protocol outlined by Murai et al (2018). The ileum and cecum were cut into sections of approximately 3 cm, inverted, closed with a string on one side, and filled with oxygen aerated Tyrode's bal-…”

Effect of delayed feeding post-hatch on expression of tight junction– and gut barrier–related genes in the small intestine of broiler chickens during neonatal development

“…Moreover, it has been shown that dietary restriction can lead to regression in mucosal development ( Uni et al., 1998 ) while MUC2 mRNA expression is reduced in intestine of germ-free birds ( Cheled-Shoval et al., 2014 ) suggesting a role of the bacterial population in mucus development. Because of the undeveloped gut barrier and immune system immediately after hatch, presence of mucus is important for gut protection during the first hours post-hatch ( Moreira Filho et al., 2019 ) and it has been suggested that enhancement of mucin secretion in young chickens during the development of the gut mucosal barrier could be beneficial in preventing the invasion of pathogenic bacteria and toxins ( Murai et al., 2018 ). Lack of feed for the first 48 h seems to have a deteriorating effect on the chicks' ability to protect itself from pathogenic bacteria and toxins.…”