MicroRNA 301A Promotes Intestinal Inflammation and Colitis-Associated Cancer Development by Inhibiting BTG1 DOI
Chong He, Tianming Yu, Yan Shi

et al.

Gastroenterology, Journal Year: 2017, Volume and Issue: 152(6), P. 1434 - 1448.e15

Published: Feb. 11, 2017

Language: Английский

Translocation of a gut pathobiont drives autoimmunity in mice and humans DOI Open Access
Sílvio M. Vieira, Michael Hiltensperger, Varun Kumar

et al.

Science, Journal Year: 2018, Volume and Issue: 359(6380), P. 1156 - 1161

Published: March 8, 2018

Bacterial involvement in autoimmunity The composition of the commensal microbiota is known to influence autoimmune disease development and persistence. Manfredo Vieira et al. identified a gut microbe, Enterococcus gallinarum , that translocates from into organs mice with genetic predisposition lupus-like (see Perspective by Citi). Molecular signatures barrier disintegration pathogenic T helper cells were evident gut, liver, lymphoid during colonization pathobiont. ensuing pathology could be reversed vancomycin treatment vaccination against E. . same bug was also found liver biopsies patients, but not healthy controls. Science this issue p. 1156 ; see 1097

Language: Английский

Citations

713

Host–microbiota interactions in immune-mediated diseases DOI
William Ruff, Teri M. Greiling, Martin Kriegel

et al.

Nature Reviews Microbiology, Journal Year: 2020, Volume and Issue: 18(9), P. 521 - 538

Published: May 26, 2020

Language: Английский

Citations

375

Intestinal epithelial claudins: expression and regulation in homeostasis and inflammation DOI
Vicky García‐Hernández, Miguel Quirós, Asma Nusrat

et al.

Annals of the New York Academy of Sciences, Journal Year: 2017, Volume and Issue: 1397(1), P. 66 - 79

Published: May 10, 2017

The intestinal epithelium forms a highly dynamic and selective barrier that controls absorption of fluid solutes while restricting pathogen access to underlying tissues. Barrier properties are achieved by intercellular junctions include an apical tight junction (TJ) subjacent adherens desmosomes. TJ tetraspan claudin proteins form pores between epithelial cells control paracellular ion movement. In addition regulation function, family members homeostasis expressed in spatiotemporal manner the crypt–luminal axis. This delicate balance physiologic differential protein expression is altered during mucosal inflammation. Inflammatory mediators influence transcriptional regulation, as well endocytic trafficking, targeting, retention claudins TJ. Increased claudin‐1, ‐2, ‐18 with downregulation claudin‐3, ‐4, ‐5, ‐7, ‐8, ‐12 has been observed inflammatory disorders. Such changes modify function influencing homeostasis. An improved understanding regulatory mechanisms will provide strategies strengthen restore

Language: Английский

Citations

363

Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders DOI Open Access
Daniel M. Chopyk, Arash Grakoui

Gastroenterology, Journal Year: 2020, Volume and Issue: 159(3), P. 849 - 863

Published: June 20, 2020

Language: Английский

Citations

326

Lactobacillus reuteri maintains intestinal epithelial regeneration and repairs damaged intestinal mucosa DOI Creative Commons
Haiqin Wu,

Shuang Xie,

Jinfeng Miao

et al.

Gut Microbes, Journal Year: 2020, Volume and Issue: 11(4), P. 997 - 1014

Published: March 5, 2020

Little is known about the regulatory effect of microbiota on proliferation and regeneration ISCs. Here, we found that L. reuteri stimulated intestinal epithelia by increasing expression R-spondins thus activating Wnt/β-catenin pathway. The proliferation-stimulating Lactobacillus repair further enhanced under TNF -induced mucosal damage, number Lgr5+ cells maintained. Moreover, compared to effects C. rodentium induction inflammation crypt hyperplasia in mice, protected barrier integrity moderately modulating signaling pathway avoid overactivation. had ability maintain stimulate epithelial damage reduce proinflammatory cytokine secretion intestine LPS concentration serum. activation also induced differentiation toward Paneth increased antimicrobial peptide inhibit colonization. protective against infection disappeared upon application Wnt antagonist Wnt-C59 both mice organoids. This study demonstrates effective at maintaining homeostasis as well repairing after pathological injury a promising alternative therapeutic method for inflammation.

Language: Английский

Citations

253

Intestinal barriers protect against disease DOI
Sandra Citi

Science, Journal Year: 2018, Volume and Issue: 359(6380), P. 1097 - 1098

Published: March 8, 2018

Leaky cell-cell junctions contribute to inflammatory and autoimmune diseases

Language: Английский

Citations

242

Microbiota‐derived extracellular vesicles in interkingdom communication in the gut DOI
Natalia Díaz‐Garrido, Josefa Badı́a, Laura Baldomà

et al.

Journal of Extracellular Vesicles, Journal Year: 2021, Volume and Issue: 10(13)

Published: Nov. 1, 2021

The intestine is fundamental in controlling human health. Intestinal epithelial and immune cells are continuously exposed to millions of microbes that greatly impact on intestinal barrier function. This microbial community, known as gut microbiota, now recognized an important partner the being actively contribute essential functions but also distal organs. In ecosystem, bidirectional microbiota-host communication does not involve direct cell contacts. Both microbiota host-derived extracellular vesicles (EVs) key players such interkingdom crosstalk. There accumulating body evidence bacterial secreted mediate by transporting delivering into host effector molecules modulate signalling pathways processes. Consequently, released may have great influence health disease. Here we review current knowledge EVs specifically highlight their role metabolism, integrity training.

Language: Английский

Citations

242

Disruption of the epithelial barrier during intestinal inflammation: Quest for new molecules and mechanisms DOI
Susana Lechuga, Andrei I. Ivanov

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2017, Volume and Issue: 1864(7), P. 1183 - 1194

Published: March 18, 2017

Language: Английский

Citations

214

The gut microbiota as a target to control hyperuricemia pathogenesis: Potential mechanisms and therapeutic strategies DOI
Jing Wang, Yong Chen, Hao Zhong

et al.

Critical Reviews in Food Science and Nutrition, Journal Year: 2021, Volume and Issue: 62(14), P. 3979 - 3989

Published: Jan. 22, 2021

Hyperuricemia (HUA) is a metabolic disorder caused by abnormal uric acid (UA) metabolism, which complex physiological process involving multiple organs (liver, kidney, and intestine). Although UA metabolism in the liver kidneys has been elucidated, only few studies have focused on intestine. With our growing knowledge of effects gut microorganisms health, microbiota identified as new target for HUA treatment. In this review, relationship between anti-hyperuricemia mechanisms targeting intestine are discussed, such promotion purine catabolism microbiota, increases excretion its metabolites, regulation absorption or secretion intestinal tract certain transporters, inflammatory response to microbiota. Additionally, probiotics (Bifidobacteria Lactobacilli) prebiotics (polyphenols, peptides, phytochemicals) with UA-lowering summarized, providing reference guidance further research.

Language: Английский

Citations

210

A human-origin probiotic cocktail ameliorates aging-related leaky gut and inflammation via modulating the microbiota/taurine/tight junction axis DOI Creative Commons
Shokouh Ahmadi, Shaohua Wang, Ravinder Nagpal

et al.

JCI Insight, Journal Year: 2020, Volume and Issue: 5(9)

Published: April 17, 2020

Inflammation is a major risk factor of morbidity and mortality in older adults. Although its precise etiology unknown, low-grade inflammation adults commonly associated with increased intestinal epithelial permeability (leaky gut) abnormal (dysbiotic) gut microbiota. The increasing population lack treatments to reduce aging-related microbiota dysbiosis, leaky gut, culminates rise comorbidities, constituting significant public health concern. Here, we demonstrate that human-origin probiotic cocktail containing 5 Lactobacillus Enterococcus strains isolated from healthy infant prevented high-fat diet–induced (HFD-induced) inflammation, metabolic dysfunctions, physical function decline mice. Probiotic-modulated primarily reduced by tight junctions, which turn inflammation. Mechanistically, probiotics modulated way increase bile salt hydrolase activity, taurine abundance the stimulated junctions suppressed leakiness. Furthermore, Caenorhabditis elegans, life span, adiposity enhanced function. results suggest such therapies could prevent or treat elderly.

Language: Английский

Citations

203