Necrotizing enterocolitis (NEC) is a severe inflammatory and necrotizing disease of the intestine that primarily affects the neonates, particularly premature infants. It has a high incidence of approximately 8.9% in extremely preterm infants, with a mortality rate ranging from 20 to 30%. In recent years, exosomes, particularly those derived from breast milk, have emerged as potential candidates for NEC therapy. Human breast milk-derived exosomes (BME) have been shown to enhance intestinal barrier function, protect intestinal epithelial cells from oxidative stress, promote the proliferation and migration of intestinal epithelial cells, and reduce the severity of experimental NEC models. As a subset of extracellular vesicles, BME possess the membrane structure, low immunogenicity, and high permeability, making them ideal vehicles for the treatment of NEC. Additionally, exosomes derived from various sources, including stem cells, intestinal epithelial cells, plants, and bacteria, have been implicated in the development and protection of intestinal diseases. This article summarizes the mechanisms through which exosomes, particularly BME, exert their effects on NEC and discusses the feasibility and obstacles associated with this novel therapeutic strategy.
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http://dx.doi.org/10.1186/s10020-024-01010-7 | DOI Listing |
Acta Histochem Cytochem
December 2024
Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi, Kitakyushu, Fukuoka 807-8555, Japan.
Inflammatory bowel disease is triggered by abnormalities in epithelial barrier function and immunological responses, although its pathogenesis is poorly understood. The dextran sodium sulphate (DSS)-induced colitis model has been used to examine inflammation in the colon. Damage to mucosa primality occurs in the large intestine and scarcely in the small intestine.
View Article and Find Full Text PDFCureus
December 2024
Department of Internal Medicine, Hasegawa Hospital, Mitaka, JPN.
Leaky gut syndrome (LGS) is caused by intestinal epithelial injury and increased intestinal permeability due to a variety of factors, including chronic stress, inflammatory bowel disease, diabetes, surgery, and chemotherapy, resulting in an increased influx of matter from the intestinal lumen causing constipation and bacteremia. To our knowledge, this is the first known case of LGS along with () bacteremia in a neurodegenerative disease patient. The patient was an 81-year-old male with a history of Alzheimer's disease, cerebral infarction, and diverticulitis in a psychiatric hospital, fed via a nasogastric tube.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Guangzhou ZhiYi Biotechnology Co. Ltd., Guangzhou, China.
() is a Gram-negative, obligate anaerobic, commensal bacterium residing in the human gut and holds therapeutic potential for ulcerative colitis (UC). Previous studies have indicated that capsular polysaccharide A (PSA) of is a crucial component for its effectiveness, possessing various biological activities such as anti-inflammatory, anti-tumor, and immune-modulating effects. We previously isolated and characterized the strain ZY-312 from the feces of a healthy breastfed infant, and extracted its PSA, named TP2.
View Article and Find Full Text PDFArq Gastroenterol
December 2024
Instituto de Ciências Biológicas da Universidade Federal de Juiz de Fora, Laboratório de Análises de Glicoconjugados, Departamento de Bioquímica, Juiz de Fora, MG, Brasil.
Chondroitin sulfate (CS) and glucosamine (GlcN) are indicated for the treatment of some inflammatory diseases, such as osteoarthritis, mainly because of the anti-inflammatory effects in reducing metalloproteinases activities (MMP), and other inflammatory mediators. Herein, we reported the structure of the CS, the anti-inflammatory and protective effects of the CS, and GlcN administration in ulcerative colitis model induced by dextran sulfate sodium (DSS) in rats. Experimental data indicated that CS disaccharide composition is very similar to the C4S standard, with modal molecular weight at 30.
View Article and Find Full Text PDFInt Immunol
January 2025
Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Several mesenchymal cell populations are known to regulate intestinal stem cell (ISC) self-renewal and differentiation. However, the influences of signaling mediators derived from mesenchymal cells other than ISC niche factors on epithelial homeostasis remain poorly understood. Here, we show that host and microbial metabolites, such as taurine and GABA, act on PDGFRαhigh Foxl1high sub-epithelial mesenchymal cells to regulate their transcription.
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