Actin cytoskeleton dynamics during mucosal inflammation: a view from broken epithelial barriers DOI
Susana Lechuga, Andrei I. Ivanov

Current Opinion in Physiology, Journal Year: 2020, Volume and Issue: 19, P. 10 - 16

Published: June 30, 2020

Language: Английский

A novel therapeutic approach for inflammatory bowel disease by exosomes derived from human umbilical cord mesenchymal stem cells to repair intestinal barrier via TSG-6 DOI
Shaopeng Yang, Xiaonan Liang, Jia Song

et al.

Stem Cell Research & Therapy, Journal Year: 2021, Volume and Issue: 12(1)

Published: May 29, 2021

Language: Английский

Citations

120

The Skin Barrier and Moisturization: Function, Disruption, and Mechanisms of Repair DOI
Jeffrey R. Rajkumar, Neha Chandan, Peter Lio

et al.

Skin Pharmacology and Physiology, Journal Year: 2023, Volume and Issue: 36(4), P. 174 - 185

Published: Jan. 1, 2023

Background: The anatomic layers of the skin are well-defined, and a functional model barrier has recently been described. Barrier disruption plays key role in several conditions, moisturization is recommended as an initial treatment conditions such atopic dermatitis. This review aimed to analyze context function model, with focus on mechanisms by which moisturizers support each promote homeostasis repair. Summary: comprised four interdependent – physical, chemical, microbiologic, immunologic maintain structure function. Moisturizers target affecting these through were shown improve transepidermal water loss studies. Occlusives, humectants, emollients occlude surface stratum corneum (SC), draw from dermis into epidermis, assimilate SC, respectively, order strengthen physical barrier. Acidic bolster chemical supporting optimal enzymatic function, increasing ceramide production, facilitating ideal for commensal microorganisms. Regular may reducing permeability subsequent allergen penetration sensitization. Key Messages: uniquely impacted states disruption. facilitate

Language: Английский

Citations

44

Intestinal mucus barrier: a missing piece of the puzzle in food allergy DOI Creative Commons
Amy Parrish, Marie Boudaud, Annette Kuehn

et al.

Trends in Molecular Medicine, Journal Year: 2021, Volume and Issue: 28(1), P. 36 - 50

Published: Nov. 19, 2021

The sudden rise in food allergy over recent decades has led to various theories including the role of environmental factors sensitization.Gastrointestinal (GI) mucins have recently been implicated maintaining gut homeostasis: mice lacking a functional mucus layer (Muc2−/− mice) are more susceptible colitis and GI infection, addition severe oral tolerance breakdown following sensitization with allergen. Thus, further research will be necessary understand how changes O-glycosylated might contribute epidemic allergy.Factors reduced consumption dietary fiber and/or increased additives emerging as key determinants altered barrier function mucin−gut microbiota interactions which appear play an important regulating allergy. prevalence allergies reached levels but cause remains largely unknown. We discuss clinical relevance mucosal site for allergic food. In this context, we focus on overlooked part pathogenesis, glycoprotein-rich layer, call attention both beneficial detrimental aspects mucus–gut microbiome interactions. Studying intricate links between barrier, associated bacteria, immune system may advance our understanding mechanisms inform prevention treatment strategies Western countries experiencing rising rates without clearly identified [1.Gupta R.S. et al.Prevalence severity among US adults.JAMA Netw. Open. 2019; 2e185630Crossref PubMed Scopus (250) Google Scholar, 2.Lyons S.A. al.Food adults: substantial variation causative foods across Europe.J. Allergy Clin. Immunol. Pract. 7: 1920-1928Abstract Full Text PDF (42) 3.Stephen-Victor E. al.Dietary microbial allergy.Immunity. 2020; 53: 277-289Abstract (10) Scholar], common include peanuts, treenuts, seafood, cow's milk. Food prevalences Europe adults were estimated at 6% 10%, respectively Scholar,2.Lyons Scholar]. allergen (see Glossary) occurs when regulatory responses fail keep up induction allergen-specific proinflammatory [3.Stephen-Victor This drastic increase researchers clinicians propose that modern lifestyles trigger Identifying underlying causually connect is upcoming area would options strategies. can manifest all ages, large spectrum symptoms profiles range from immediate IgE-mediated delayed non-IgE-mediated [4.Connors L. al.Non-IgE-mediated hypersensitivity.Allergy, Asthma 2018; 14: 56Crossref (22) Scholar,5.Anvari S. al.IgE-mediated allergy.Clin. Rev. 57: 244-260Crossref Sensitization allergens initiation disease begin sites share protective features such cohesive epithelium overlies dynamic (Figure 1). 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I. Gastrointestinal different depending location well Peyer's patches.Am. Physiol. Gastrointest. Liver 2013; 305: G341-G347Crossref (197) Scholar] 2). Moreover, structure composition varies along length parallel morphology mucin-5AC (MUC5AC) predominant gel-forming structured two thick firmly adherent attached overlain loose [28.Atuma gel layer: thickness physical vivo.Am. 2001; 280: G922-G929Crossref These work buffer facilitate proton secretion protecting gastric tissue acidic content [29.Lewis O.L. physics-based pH gradient layer.Am. 2017; 313: G599-G612Crossref (12) intestines, mucin-2 (MUC2) mucin, although structures intestine single permits commensals enter closer these sampled lamina propria antigen-presenting [30.Shan al.Mucus homeostasis delivering immunoregulatory signals.Science. 342: 447-453Crossref (342) By contrast, colon, distinct described, outer being whereas inner one impermeable Scholar,31.Johansson colon MUC2 legislator host-microbial interactions.Proc. U. 108: 4659-4665Crossref (740) Indeed, MUC2-deficient display thinner looser come proximity [32.Wenzel U.A. al.Spontaneous Muc2-deficient reflects cellular ulcerative colitis.PLoS One. 9e100217Crossref (56) reported develop spontaneous even absence [33.Van der Sluis al.Muc2-deficient spontaneously colitis, indicating critical protection.Gastroenterology. 2006; 131: 117-129Abstract (940) Scholar,34.Van Paassen N.B. al.Colitis suckling-weaning transition muc2-deficient mice.Am. 301: G667-G678Crossref (23) addition, they show high susceptibility tumors driven low-grade inflammation proliferative cells, demonstrating preserving [35.Velcich al.Colorectal cancer genetically deficient Muc2.Science. 2002; 295: 1726-1729Crossref (666) Scholar,36.Tadesse al.MUC2 deficiency alters metabolic pathways mucosa.Oncotarget. 8: 71456-71470Crossref protein backbone O-glycosylation viscoelasticity mucus, thus promoting its expel particles, parasites [37.Bergstrom al.Proximal colon-derived encapsulates modulates microbiota.Science. 370: 467-472Crossref Scholar,38.Sharpe sticky end helminths; barrier.Parasite 40e12517Crossref allergens. four main types O-glycan structural cores, terminal fucosylation, sialylation, sulfation, post-translational modifications differentially distributed [11.Martens Scholar,39.Robbe al.Structural distribution O-glycans normal human tract.Biochem. 2004; 384: 307-316Crossref (229) It was shown differential patterning glycosylation proximal distal governs formation two-layered optimal exclusion fecal pellets conformation their proteolysis enzymes [40.Bergstrom al.Core 1- 3-derived collectively maintain mice.Mucosal 10: 91-103Crossref (62) Scholar,41.Van Der Post al.Site-specific inhibits cleavage Porphyromonas gingivalis cysteine protease (RgpB).J. Chem. 288: 14636-14646Abstract (57) Consistently, defects disorganized microbiota-dependent Scholar,42.Fu al.Loss core 1-derived mice.J. 121: 1657-1666Crossref (231) Scholar,43.Tobisawa Y. al.Sulfation N-acetylglucosamine 6-O-sulfotransferase-2 experimental 285: 6750-6760Abstract (63) Recent characterization MUC2+ single-cell RNA-seq subpopulations GCs differ based gene expression profiles, localization patterns [44.Nyström E.E.L. al.An intercrypt subpopulation function.Science. 372eabb1590Crossref crypt- intercrypt-derived generate impenetrable bacteria-sized 1 μm beads However, 0.2 2000 kDa fluorescein-labeled dextran, mimicking nutrients, could only penetrate mucus. Intriguingly, populations distinguished lectin staining, revealing study paves way towards high-resolution interface system. Mucin production regulated products described type 2 elicited parasite induce GC hyperplasia IL-13–IL-4Rα–STAT6 pathway [38.Sharpe Scholar,45.Oeser al.Conditional IL-4/IL-13-deficient reveal innate immunity helminths.Mucosal 672-682Crossref cholinergic agonists, histamine prostaglandin E2 released effector inducers intestines [46.Halm Halm S.T. Secretagogue response columnar crypts.Am. Phys. 2000; 278: C212-C233Crossref Scholar,47.Specian R.D. Neutra M.R. Mechanism rapid stimulated acetylcholine.J. Cell 1980; 85: 626-640Crossref Although found allergy, little known subsequent outcome composition. depletion food-allergic patients proctitis [48.Carroccio al.Chronic constipation intolerance: constipation.Scand. Gastroenterol. 2005; 40: 33-42Crossref replenishment observed after avoidance, suggesting allergen-driven contrasts IL-13-driven overproduction pathological [49.Lambrecht B.N. cytokines asthma.Immunity. 50: 975-991Abstract (249) Colonic also (UC, disease, IBD) sentinel entrance crypts do not produce bacterial stimuli, contrast healthy controls remission [50.Van weakening early event pathogenesis.Gut. 68: 2142-2151Crossref (79) revealed UC those exhibit decreased GCs, leaving areas uncovered exposed Studies models demand synthesis leads endoplasmic reticulum (ER) stress apoptosis, turn release [51.Heazlewood C.K. al.Aberrant assembly resembling 2008; 5e54Crossref (493) Scholar,52.Tawiah al.High misfolding stress, reactive oxygen production, apoptosis cells.Am. Pathol. 188: 1354-1373Abstract thought follow discharge induced stimulation inflammation, initiating process remain unclear. helper cell (Th2) cytokines, Th1 Th17 controversial, level regulation. (including etiologically diseases, coexist [53.Virta L.J. al.Cow's milk pediatric IBD.J. Pediatr. Nutr. 56: 649-651Crossref 54.Cai al.Serological investigation G antibodies diseases.PLoS 9e112154Crossref (31) 55.Wasielewska Z. children disease.Postep. Dermatologii i Alergol. 36: 286-294Crossref Children protein-induced enterocolitis (FPIE), endotype allergies, low anti-inflammatory receptor TGFβRI cytokine TNF-α [56.Chung H.L. al.Expression transforming growth β1, I II receptors, mucosa syndrome.J. 109: 150-154Abstract (153) permeability mediate IBD [57.Michielan D'Incà R. Intestinal disease: evaluation, therapy leaky gut.Mediat. Inflamm. 2015: 628517Crossref (243) it together TGF-β signal transduction favor antigen translocation considered affect principally downregulating tight junction proteins, impact studied extensively. pups, TNFRI-dependent manner Muc2 mRNA TNFRII-dependent [58.McElroy S.J. al.Tumor necrosis 1-dependent immature intestine: neonatal necrotizing enterocolitis.Am. 656-666Crossref Scholar]; developed postnatal period. Cytokine-induced ileum emerged TNFRI-mediated secretion, TNFRII-mediated effective mature complexity studying expression, emphasizes need explore levels. mucus-secreting lines, [59.Iwashita al.mRNA

Language: Английский

Citations

58

Epithelial barrier dysfunction in ocular allergy DOI

Neera Singh,

Yolanda Diebold, Srikant Kumar Sahu

et al.

Allergy, Journal Year: 2021, Volume and Issue: 77(5), P. 1360 - 1372

Published: Nov. 10, 2021

The epithelial barrier is the first line of defense that forms a protective against pathogens, pollutants, and allergens. Epithelial dysfunction has been recently implicated in development allergic diseases such as asthma, atopic dermatitis, food allergy, rhinitis. However, there limited knowledge on ocular allergy (OA). Since surface directly exposed to environment, it important understand role epithelia their OA. Impaired enhances allergen uptake, which lead activation immune responses chronic inflammation seen allergies. Abnormal expression tight junction proteins helps maintain integrity reported OA but sufficient data not available (AKC) vernal keratoconjunctivitis (VKC), pathophysiology just complex, also current treatments are completely effective. This review provides an overview studies, indicates OA, highlights how possibly contributes disease pathogenesis. explores potential repair strategies preventive therapeutic approach.

Language: Английский

Citations

57

The Ability of Resveratrol to Attenuate Ovalbumin-Mediated Allergic Asthma Is Associated With Changes in Microbiota Involving the Gut-Lung Axis, Enhanced Barrier Function and Decreased Inflammation in the Lungs DOI Creative Commons

Esraah Alharris,

Amira Mohammed, Hasan Alghetaa

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Feb. 21, 2022

Asthma is a chronic respiratory disease highly prevalent worldwide. Recent studies have suggested role for microbiome-associated gut-lung axis in asthma development. In the current study, we investigated if Resveratrol (RES), plant-based polyphenol, can attenuate ovalbumin (OVA)-induced murine allergic asthma, and so, of microbiome this process. We found that RES attenuated with significant improvements pulmonary functions OVA-exposed mice when tested using plethysmography frequency (F), mean volume (MV), specific airway resistance (sRaw), delay time(dT). treatment also suppressed inflammatory cytokines lungs. modulated lung microbiota caused an abundance Akkermansia muciniphila accompanied by reduction LPS biosynthesis OVA-treated mice. Furthermore, altered gut induced enrichment Bacteroides acidifaciens significantly colon increase butyric acid concentration colonic contents from Additionally, increases tight junction proteins decreased mucin (Muc5ac) epithelium Our results demonstrated may inducing beneficial through promotion normal barrier lung.

Language: Английский

Citations

52

The role of intestinal microbes on intestinal barrier function and host immunity from a metabolite perspective DOI Creative Commons

Yi-Feng Fu,

Jin Lyu,

Shuangshuang Wang

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Oct. 9, 2023

The gut is colonized by many commensal microorganisms, and the diversity metabolic patterns of microorganisms profoundly influence intestinal health. These microbial imbalances can lead to disorders such as inflammatory bowel disease (IBD). Microorganisms produce byproducts that act signaling molecules, triggering immune system in mucosa controlling inflammation. For example, metabolites like short-chain fatty acids (SCFA) secondary bile release inflammatory-mediated signals binding specific receptors. indirectly affect host health immunity interacting with epithelial mucosal cells. Moreover, Tryptophan-derived also play a role governing response aromatic hydrocarbon receptors (AHR) located on mucosa, enhancing barrier. Dietary-derived indoles, which are synthetic precursors AHR ligands, work together SCFA reduce stress epithelium regulate This review highlights interaction between system, well crosstalk dietary fiber intake improving metabolism its beneficial effects organism.

Language: Английский

Citations

42

Understanding disruption of the gut barrier during inflammation: Should we abandon traditional epithelial cell lines and switch to intestinal organoids? DOI Creative Commons
Susana Lechuga, Manuel B. Braga Neto, Nayden G. Naydenov

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 16, 2023

Disruption of the intestinal epithelial barrier is a hallmark mucosal inflammation. It increases exposure immune system to luminal microbes, triggering perpetuating inflammatory response. For several decades, stimuli-induced breakdown human gut was studied in vitro by using colon cancer derived cell lines. While providing wealth important data, these lines do not completely mimic morphology and function normal cells (IEC) due cancer-related chromosomal abnormalities oncogenic mutations. The development organoids provided physiologically-relevant experimental platform study homeostatic regulation disease-dependent dysfunctions barrier. There need align integrate emerging data obtained with classical studies that utilized This review discusses utilization dissect roles mechanisms disruption during We summarize available generated two major types from either crypts or induced pluripotent stem compare them results earlier conventional identify research areas where complementary use cancer-derived advance our understanding inflamed unique questions could be addressed only organoid platforms.

Language: Английский

Citations

34

Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases DOI Creative Commons
Andrea Padoan, Giulia Musso, Nicole Contran

et al.

Current Issues in Molecular Biology, Journal Year: 2023, Volume and Issue: 45(7), P. 5534 - 5557

Published: June 30, 2023

In this review, the role of innate and adaptive immunity in pathogenesis inflammatory bowel diseases (IBD) is reported. IBD, an altered often found, with increased Th17 decreased Treg cells infiltrating intestinal mucosa. An associated increase cytokines, such as IL-1 TNF-α, a decrease anti-inflammatory IL-10, concur favoring persistent inflammation gut Autoinflammation highlighted insights inflammasomes, which activation by exogenous or endogenous triggers might be favored mutations NOD NLRP proteins. Autoimmunity mechanisms also take place IBD context immune stimulation bacterial antigens derived from degradation, response takes results antibodies autoantibodies production, frequent finding these diseases. Inflammation, autoinflammation autoimmunity altering mucus layer enhancing permeability, sustains vicious cycle further mucosal inflammation.

Language: Английский

Citations

33

Butyrate suppresses atherosclerotic inflammation by regulating macrophages and polarization via GPR43/HDAC-miRNAs axis in ApoE−/− mice DOI Creative Commons

Huiyan Ma,

Libo Yang, Yajuan Liu

et al.

PLoS ONE, Journal Year: 2023, Volume and Issue: 18(3), P. e0282685 - e0282685

Published: March 8, 2023

Chronic low-grade inflammation is regarded to an important signature of atherosclerosis (AS). Macrophage (Mψ) and related polarization have been demonstrated play a crucial role in the occurrence development AS inflammation. Butyrate, bioactive molecule produced by intestinal flora, has increasingly exhibit vital for regulating chronic metabolic diseases. However, effectiveness multiple anti-inflammation mechanisms butyrate on still need be further understood. ApoE −/− mice fed with high-fat diet as model were administered sodium (NaB) 14 weeks treatment. Our results showed that atherosclerotic lesion group was dramatically reduced after NaB intervention. Moreover, deteriorated routine parameters including body weights (BWs), low-density lipoprotein (LDL-C), triglyceride (TG), total cholesterol (TC) significantly reversed administration. Abnormal elevated plasma aorta pro-inflammatory indicators interleukin (IL)-1β, IL-6, IL-17A, tumor necrosis factor (TNF)-α lipopolysaccharide (LPS), well anti-inflammatory IL-10 respectively rectified Consistently, accumulated Mψ associated imbalance arota attenuated Importantly, we suppression dependent binding G-protein coupled receptor (GPR) inhibiting histone deacetylase HDAC3. found butyrate-producing bacteria, bacteria tight junction protein zonula occludens-1 (ZO)-1 may contribute this effectiveness. Intriguingly, according transcriptome sequencing aorta, 29 24 miRNAs treatment, especially miR-7a-5p, suggesting non-coding RNA possess potential protection against AS. Correlation analysis there close complicated interactions among gut microbiota, differential miRNAs. Collectively, study revealed dietary ameliorate via GPR43/HDAC-miRNAs axis mice.

Language: Английский

Citations

29

Gut Microbiota Dysbiosis as One Cause of Osteoporosis by Impairing Intestinal Barrier Function DOI
Ning Wang, Sicong Ma,

Lingjie Fu

et al.

Calcified Tissue International, Journal Year: 2021, Volume and Issue: 110(2), P. 225 - 235

Published: Sept. 4, 2021

Language: Английский

Citations

54