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Parenteral and Enteral Nutrition in Critical Illness
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Most clinicians now agree that enteral feeding is the preferred route for the critically ill. Early enteral nutrition increases crosstalk signaling between the bowel flora and intestinal cells. Bacterial binding to Toll-like and Nod-like receptors on the intestinal epithelium improves gut barrier defenses. In the case of intestinal epithelial cell bacterial binding, enteral nutrition increases expression of tight junction proteins. In goblet cells, it increases mucus production. In Paneth cells, it increases the release of Defensins to bind pathogens. In dendritic cells, it influences T-cell differentiation.
Role of Lectins in Gastrointestinal Disorders
Published in Megh R. Goyal, Preeti Birwal, Durgesh Nandini Chauhan, Herbs, Spices, and Medicinal Plants for Human Gastrointestinal Disorders, 2023
Lectins are proteins derived largely from plants and some animals, that they bind to specific sugar residues in tissues including the intestinal tract. Using lectin histochemical methods, the gastrointestinal tract has been explored to define the location of carbohydrate-containing structures. In addition, there are alterations in disease states, including the poorly differentiated, but nonmalignant, epithelial cells in celiac disease, and malignant intestinal epithelial cell disorders in cancer.
The Silver Lining
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Mark R Frey, Misty Good, Steven J. McElroy
Goblet cells are the major secretory cell located in the intestinal epithelium and are responsible for producing trefoil peptides, resistin-like molecule-β, Fcγ binding protein, and mucin (mucus) (85). Intestinal mucus is one of the key components of innate immunity (Figure 39.4) (86). Mucins are large glycoproteins that provide a physical barrier, facilitate removal of adherent bacteria, and aid in host nutrient digestion (87). They are expressed early in development and reach adult levels by 27 weeks of gestation (88). However, the mucus produced by immature intestinal tracts has different viscosity (89), buoyancy, and carbohydrate composition (90) than in adults.
Human milk oligosaccharide disialyllacto-n-tetraose protects human intestinal epithelium integrity and permeability against mast cell chymase-induced disruption by stabilizing ZO-1/FAK/P38 pathway of intestinal epithelial cell
Published in Immunopharmacology and Immunotoxicology, 2023
Xuejiao Lian, Wenting Zhang, Jingqiu He-Yang, Xiaoying Zhou
Inflammatory bowel diseases (IBD), including ulcerative colitis (UC), Crohn’s disease (CD) and necrotizing enterocolitis (NEC) [1], are chronic immune-mediated gut diseases associated with intestinal epithelium damage [2]. The enteral epithelium is a single-cell layer as a physical barrier for selectively absorbing nutrients, electrolytes, and water, as well as an effective defense system against endovascular toxins, antigens, and intestinal flora [3,4]. Intestinal epithelial permeability is regulated by a complex protein system comprising a tight junction (TJ) for cell-cell connection [5] including adherent junctional proteins, such as E-cadherin, occludin, and zonula occludens (ZO). Zonula occludens-1 (ZO-1), a tight junction protein, contributes to the maintenance of the polarity of epithelial cells and junctional complex formation in the epithelium layer. ZO-1 binds directly to actin filaments and mainly regulates cell cytoskeleton arrangement [6]. FAK (Focal Adhesion Kinase or PTK2) is a widely expressed cytosolic tyrosine kinase that is involved in integrin signaling and regulates the sites of cell-matrix adhesion [7,8]. P38 signaling interactive pathway is one of the mitogen-activated protein kinase (MAPK) signaling pathways, and is responsible for regulating a variety of cellular activities, including proliferation, differentiation, and apoptosis, in response to certain environmental stimuli.
Colon specific delivery of miR-155 inhibitor alleviates estrogen deficiency related phenotype via microbiota remodeling
Published in Drug Delivery, 2022
Lianbi Zhao, Tian Zhou, Jianmei Chen, Wenbin Cai, Ruijing Shi, Yunyou Duan, Lijun Yuan, Changyang Xing
Regarding the easy manipulation and targetable traits of miRNAs, we explored the possibility of colon specific delivery of miR-155 antagonist in restoring the microbiota dysbiosis and the associated cardiac dysfunction. The Eudragit S100 coating microsphere is intact in the stomach and intestine and thus protects the miRNA antagonists from degradation in the stomach and small intestine, resulting in specific release of the miRNAs in the colon (Jose et al., 2011). Compared with microbial transplantation, colon specific miRNA delivery-based microbiota restoration has multiple advantages. 1) The intestinal epithelium and the intestinal mucosal barrier that it secretes play a supportive role for the gut flora establishment (Faderl et al., 2015). Bacterium transplantation alone without supportive environment reconstruction might only have transient effects. However, targeting the mechanism how microbiota changes, might reestablish the microbial ecosystem from the preexisting microbiota. 2) Regarding the fecal origin, delivery of microbiota or specific bacterium is psychologically difficult for certain patients. In addition, as a live organism, the bacterium is difficult for manipulation, expansion, and transportation (Browne et al., 2016). In contrast, microsphere or other colon specific delivery strategies based miRNA delivery would overcome all of these disadvantages.
Gut microbiota-motility interregulation: insights from in vivo, ex vivo and in silico studies
Published in Gut Microbes, 2022
Barbora Waclawiková, Agnese Codutti, Karen Alim, Sahar El Aidy
Gut hormones are released from specialized intestinal epithelial cells, enteroendocrine cells, in response to meal-related stimuli. Subsequently, these gut hormones exert actions ranging from the local control of gut motility, to the regulation of glucose homeostasis, and food intake.68 Gastrointestinal motility is modulated by gut hormones during both the interdigestive (i.e. between meals; motilin and ghrelin), and postprandial (i.e. after meals; cholecystokinin (CCK), glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY)) periods.69 GLP-1, and PYY are key mediators of the shift from an interdigestive to a postprandial gastrointestinal motor pattern.69 Moreover, the gut hormones CCK, GLP-1, and PYY control blood nutrient levels by modulating digestion and absorption, as slowing either of these steps reduces the rate at which ingested nutrients enter the circulation.68