Abstract
Dietary supplementation with spray-dried porcine plasma (SDP) can modulate the immune response of gut-associated lymphoid tissue. SDP supplementation reduces acute mucosal inflammation, as well as chronic inflammation associated with aging. The aim of this study was to analyze if SDP supplementation could ameliorate colitis in a genetic mouse model of inflammatory bowel disease (IBD). Wild-type mice and Mdr1a knockout (KO) mice were administered a control diet or an SDP-supplemented diet from day 21 (weaning) until day 56. The histopathological index, epithelial barrier, and intestinal immune system were analyzed in the colonic mucosa. KO mice had higher epithelial permeability, increased Muc1 and Muc4 expression, and lower abundance of E-cadherin and Muc2 (all p < 0.001). SDP prevented these effects (all p < 0.05) and decreased the colonic inflammation observed in KO mice, reducing neutrophil and monocyte infiltration and activation and the percentage of activated T helper lymphocytes in the colonic mucosa (all p < 0.05). SDP also diminished proinflammatory cytokine expression and increased the anti-inflammatory IL-10 concentration in the colonic mucosa (all p < 0.05). In conclusion, dietary supplementation with SDP enhances colon barrier function and reduces mucosal inflammation in a mouse model of IBD.
Highlights
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract that is classically divided into Crohn disease and ulcerative colitis
Using the Mdr1a knockout (KO) mouse model of colitis [10,11], we previously showed that serum-derived bovine immunoglobulins (SBI) reduce colon permeability and the expression of oxidative markers and proinflammatory cytokines in the colonic mucosa, as well as leukocyte infiltration in the lamina propria and mesenteric lymph nodes [12,13]
Histopathological and disease activity indices were increased in colitic mice and spray-dried porcine plasma (SDP) supplementation had no significant effects
Summary
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract that is classically divided into Crohn disease and ulcerative colitis. In IBD, which is characterized by alternative recurrence and alleviation periods, patients suffer from abdominal pain, diarrhea, bloody stools, and weight loss [1]. It is a global disease, with increasing incidence and prevalence around the world [2]. The intestinal inflammatory response in patients with IBD involves deregulation of gut-associated lymphoid tissue (GALT) [4] This tissue is divided into inductive sites, which include the mesenteric lymph nodes, Peyer’s patches (in the small intestine), colonic patches, and isolated lymphoid follicles, and into effector sites, which include intraepithelial lymphocytes and lymphocytes from the lamina propria [5]. In IBD patients, the integrity of the epithelial barrier is compromised, as shown by increased paracellular permeability and lower levels of tight junction proteins [8]
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