Role of the Mucosal Barrier in Toxin/Microbial Attachment to the Gastrointestinal Tract

Walker, W. Allan

doi:10.1002/9780470720936.ch3

Cited by 9 publications

(4 citation statements)

References 53 publications

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“…SIBO is characterized with the small intestinal excessive numbers and types of bacteria overgrowth exceeding 10 5 organisms/mL, which are mainly colonic type with predominantly gram-negative aerobic species ( Streptococcus , Escherichia coli, staphylococcus ) and anaerobic species ( Lactobacillus, bacteroides, clostridium and veillonella )[ 118 ]. Enterotoxins expressing in the outer membrane of germ-negative species can damage the intestinal mucosa barrier by stimulation of fluid secretion in enterocytes, and further affect the absorptive function[ 119 ]. SIBO is associated with irritable bowel syndrome (IBS), celiac disease (CD) as well as IBD[ 120 ], and also involved in the development of nonalcoholic fatty liver disease[ 121 ].…”

Section: Microbiota Utilization Of Diet Microbiota Metabolites and The Role Of Microbiota In The Liver-gut Axismentioning

confidence: 99%

Fatty acid metabolism and acyl-CoA synthetases in the liver-gut axis

Ma¹,

Nenkov²,

Chen³

et al. 2021

WJH

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Fatty acids are energy substrates and cell components which participate in regulating signal transduction, transcription factor activity and secretion of bioactive lipid mediators. The acyl-CoA synthetases (ACSs) family containing 26 family members exhibits tissue-specific distribution, distinct fatty acid substrate preferences and diverse biological functions. Increasing evidence indicates that dysregulation of fatty acid metabolism in the liver-gut axis , designated as the bidirectional relationship between the gut, microbiome and liver, is closely associated with a range of human diseases including metabolic disorders, inflammatory disease and carcinoma in the gastrointestinal tract and liver. In this review, we depict the role of ACSs in fatty acid metabolism, possible molecular mechanisms through which they exert functions, and their involvement in hepatocellular and colorectal carcinoma, with particular attention paid to long-chain fatty acids and small-chain fatty acids. Additionally, the liver-gut communication and the liver and gut intersection with the microbiome as well as diseases related to microbiota imbalance in the liver-gut axis are addressed. Moreover, the development of potentially therapeutic small molecules, proteins and compounds targeting ACSs in cancer treatment is summarized.

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Section: Microbiota Utilization Of Diet Microbiota Metabolites and The Role Of Microbiota In The Liver-gut Axismentioning

confidence: 99%

Fatty acid metabolism and acyl-CoA synthetases in the liver-gut axis

Ma¹,

Nenkov²,

Chen³

et al. 2021

WJH

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“…Supplementation of formula with EGF reduced intestinal epithelial cell apoptosis in the ileum (71). Perturbation of the intestinal barrier has been implicated in the pathogenesis of NEC (45, 72-74). A recent study from our laboratory has shown that intestinal permeability, ileal goblet cell density, and mucin production are altered in rats with NEC (59).…”

Section: Egf In Necmentioning

confidence: 99%

Milk Epidermal Growth Factor and Gut Protection

Dvořák

2010

The Journal of Pediatrics

121

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Maternal milk is a complex fluid with multifunctional roles within the developing gastrointestinal tract. Epidermal growth factor (EGF) and heparin-binding EGF-like growth factor (HB-EGF) are members of the family of EGF-related peptides. Biological actions of these growth factors are mediated via interaction with the EGF-receptor (EGF-R). In the early postnatal period, breast milk is the major source of EGF for the developing intestinal mucosa. HB-EGF is also detected in breast milk, but in concentrations 2 to 3 times lower than EGF. Under normal physiological conditions, the intestinal epithelium undergoes a continuing process of cell proliferation, differentiation and maturation. EGF plays an important role in these processes. In pathophysiologic situations, EGF contributes to epithelial protection from injury and post-injury mucosal repair. Necrotizing enterocolitis (NEC) is a devastating disease affecting prematurely born infants. The pathogenesis of NEC is not known and there is no effective treatment for this disease. In an experimental NEC model, oral administration of a physiological dose of EGF significantly reduces the incidence and severity of NEC. HB-EGF provides similar protection against NEC, but only when pharmacological doses are used. Further studies are necessary before EGF can be introduced as an efficient therapeutic approach of intestinal injury. Maternal milk and developing gutMaternal milk is an important and well-balanced source of nutrition for the newborn (1). Milk provides not only major nutrients, vitamins and minerals, but also a plethora of biologically active substances, such as hormones, cytokines, and growth factors (2-6). These biological active factors not only facilitate the development of essential digestive functions, but also regulate the maturation of the intestinal mucosal barrier (7). In addition to their normal physiological functions, many of these factors have the capacity to stimulate the healing and repair processes in injured intestinal epithelium.The gastrointestinal (GI) tract is a complex organ which undergoes substantial changes during the early stages of development. Profound growth, morphological and functional changes are observed during the late gestation and early postnatal period (8). Birth is possibly the most critical period in gastrointestinal development, when placental supply is replaced by enteral nutrition. Enteral nutrition initiates changes in intestinal mucosal structure and function required for utilization of milk feedings. However, intestinal maturation begins long before birth and amniotic fluid plays an important role in this process (7). In addition to its digestive

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“…Perturbation of the intestinal barrier has been implicated in the pathogenesis of NEC (31)(32)(33)(34), and a recent study from our laboratory has shown that intestinal permeability, ileal goblet cell density, and mucin production are altered in rats with NEC (11). Because HB-EGF and EGF have been associated with improved intestinal barrier function (35,36), we evaluated structural and functional changes of the intestinal barrier in rats treated with HB-EGF, EGF, or EþHB.…”

Section: Discussionmentioning

confidence: 99%