Digestive and Liver Disease, Год журнала: 2023, Номер 56(6), С. 911 - 922
Опубликована: Ноя. 25, 2023
Язык: Английский
International Journal of Oral Science, Год журнала: 2022, Номер 14(1)
Опубликована: Март 2, 2022
Abstract Oral bacteria directly affect the disease status of dental caries and periodontal diseases. The dynamic oral microbiota cooperates with host to reflect information immunity metabolism through two-way communication along cavity systemic organs. is one most important interaction windows between human body environment. microenvironment at different sites in has microbial compositions regulated by complex signaling, hosts, external environmental factors. These processes may or health because certain states seem be related composition bacteria, destruction community In this review, we discussed emerging exciting evidence connections microbes multiple diseases, possible contribution microorganisms This review aims enhance interest on whole body, also improve clinician’s understanding role Microbial research dentistry potentially enhances our knowledge pathogenic mechanisms same time, continuous advances frontier field lead a tangible impact health.
Язык: Английский
Процитировано
341
Frontiers in Cellular and Infection Microbiology, Год журнала: 2022, Номер 12
Опубликована: Фев. 22, 2022
Epidemiological surveys indicate that the incidence of inflammatory bowel disease (IBD) is increasing rapidly with continuous growth economy. A large number studies have investigated relationship between genetic factors related to susceptibility IBD and gut microbiota patients by using high-throughput sequencing. considered outcome interaction host microorganisms, including intestinal microbial factors, abnormal immune response, a damaged mucosal barrier. The imbalance homeostasis leads colonization invasion opportunistic pathogens in gut, which increases risk response promotes development IBD. It critical identify specific pathogenesis An in-depth understanding various pathogenic great significance for early detection This review highlights role provides theoretical basis personalized approaches modulate treat
Язык: Английский
Процитировано
274
Frontiers in Immunology, Год журнала: 2021, Номер 12
Опубликована: Ноя. 11, 2021
In inflammatory bowel disease (IBD), intestinal mucosa cell and epithelial are severely damaged, then their susceptibility to bacteria increases, so many commensal become pathogenic. The pathogenic can stimulate a series of compensatory immune responses in the intestine. However, response prevents tract from restoring homeostasis, which turn produces an indispensable response. On contrary, IBD, fierce contributes development IBD. effect on inflammation IBD has not been clearly studied. Therefore, we further summarize changes brought about by intestines mutual influence. This article reviews protective mechanism healthy people destruction barrier when occurs. treatment prevention also briefly summarized.
Язык: Английский
Процитировано
153
International Journal of Oral Science, Год журнала: 2022, Номер 14(1)
Опубликована: Июнь 23, 2022
Abstract The aim of this study was to identify whether periodontitis induces gut microbiota dysbiosis via invasion by salivary microbes. First, faecal and samples were collected from periodontally healthy participants (PH group, n = 16) patients with severe (SP 21) analysed 16S ribosomal RNA sequencing. Significant differences observed in both the between PH SP groups. Notably, more saliva-sourced microbes group. Then, remaining transplanted into C57BL6/J mice (the C-PH group C-SP group), it found that composition significantly different Porphyromonadaceae Fusobacterium being enriched In colon, showed reduced crypt depth zonula occludens-1 expression. mRNA expression levels pro-inflammatory cytokines, chemokines tight junction proteins higher To further investigate bacteria could persist intestine, stained carboxyfluorescein diacetate succinimidyl ester mice. We for at least 24 h. Thus, our data demonstrate may induce through influx
Язык: Английский
Процитировано
115
Gastroenterology, Год журнала: 2023, Номер 166(1), С. 44 - 58
Опубликована: Сен. 20, 2023
The gut microbiota plays a significant role in the pathogenesis of both forms inflammatory bowel disease (IBD), namely, Crohn's (CD) and ulcerative colitis (UC). Although evidence suggests dysbiosis loss beneficial microbial species can exacerbate IBD, many new studies have identified microbes with pathogenic qualities, termed "pathobionts," within intestines patients IBD. concept pathobionts initiating or driving chronicity IBD has largely focused on putative aggravating that adherent invasive Escherichia coli may play CD. However, recent additional bacterial fungal CD UC. This review will highlight characteristics these their implications for treatment. Beyond exploring origins pathobionts, we discuss those associated specific clinical features potential mechanisms involved, such as creeping fat (Clostridium innocuum) impaired wound healing (Debaryomyces hansenii) well increased fecal proteolytic activity (Bacteroides vulgatus) seen biomarker UC severity. Finally, examine impact current therapies, several approaches to target currently early stages development. Despite recognizing likely contribute more work is needed define modes action. Determining whether causal relationships exist between could pave way improved care patients, particularly not responding therapies. incidence diseases (IBD; [CD] [UC]), increasing most industrialized countries.1Ng S.C. Shi H.Y. Hamidi N. et al.Worldwide prevalence 21st century: systematic population-based studies.Lancet. 2017; 390: 2769-2778Abstract Full Text PDF PubMed Scopus (3342) Google Scholar etiology complex, it thought reflect dysregulated immunity develops genetically susceptible individuals after exposure noxious environmental stimuli, including microbes. Genome-wide association than 200 genes2Ye B.D. McGovern D.P.B. Genetic variation IBD: progress, clues possible utility.Expert Rev Clin Microbiol. 12: 1091-1107Google Scholar,3Peters L.A. Perrigoue J. Mortha A. al.A functional genomics predictive network model identifies regulators disease.Nat Genet. 49: 1437-1449Crossref (151) (eg, NOD2, ATG16L1), encoding key proteins underlying host processes aimed at controlling eliminating invading microbes, autophagy, oxidative stress, epithelial barrier integrity, Paneth immune cell functions.4Hampe Franke Rosenstiel P. genome-wide scan nonsynonymous SNPs susceptibility variant Crohn ATG16L1.Nat 2007; 39: 207-211Crossref (1596) Scholar,5Hugot Chamaillard M. Zouali H. al.Association NOD2 leucine-rich repeat variants disease.Nature. 2001; 411: 599-603Crossref (4813) Only 19%–26% heritability explained by genetics,3Peters suggesting factors, bacteria, promote even without genetic susceptibility. Interestingly, prior acute infection enteric pathogens related antibiotic exposures been repeatedly shown be risk factors IBD.6Faye A.S. Allin K.H. Iversen A.T. al.Antibiotic use factor across ages: cohort study.Gut. 2023; 72: 663-670Crossref (16) they are unlikely directly because typically precede development years. Intestinal well-established feature IBD.7Gevers D. Kugathasan S. Knights Microbiome Foundation Study Disease.Cell Host Microbe. 21: 301-304Abstract (37) Scholar,8Michail Durbin Turner al.Alterations microbiome children severe colitis.Inflamm Bowel Dis. 2013; 18: 1799-1808Google Previously defined "compositional alterations [driven by] host-related factors,"9Levy Kolodziejczyk A.A. Thaiss C.A. al.Dysbiosis system.Nat Immunol. 17: 219-232Crossref (947) caused inflammation, infection, genetics, dietary habits characterized one following: blooms potentially an overall diversity.9Levy Scholar,10Tiffany C.R. Bäumler A.J. Dysbiosis: from fiction function.Am J Physiol - Gastrointest Liver Physiol. 2019; 317: G602-G608Crossref (0) often found bidirectional nature intestinal inflammation concurrent only recently investigated. Historically, recruited analysis relative healthy controls, displaying reduced diversity temporal compositional variability.11Matsuoka K. Kanai T. disease.Semin Immunopathol. 2015; 37: 47-55Crossref (532) Scholar, 12Kostic A.D. Xavier R.J. Gevers disease: status future ahead.Gastroenterology. 2014; 146: 1489-1499Abstract (1235) 13Ryan F.J. Ahern A.M. Fitzgerald R.S. al.Colonic epigenomic Commun. 2020; 11: 1-12Crossref (147) 14Clooney A.G. Eckenberger Laserna-Mendieta E. al.Ranking variance large longitudinal intercontinental 2021; 70: 499-510Crossref (109) To further clarify dysbiotic compared present paired inflamed noninflamed tissues Most differences taxa sites Enterobacteriaceae Bacteroides decreased Firmicutes), however, varied same study.13Ryan Scholar,15Hirano Umeno Okamoto Y. al.Comparison community structure non-inflamed colitis.J Gastroenterol Hepatol. 2018; 33: 1590-1597Crossref (77) 16Moen A.E.F. Lindstrøm J.C. Tannæs T.M. al.The transcriptional mucosal patients.Sci Rep. 8: 1-12Google 17Walker A.W. Sanderson J.D. Churcher C. al.High-throughput clone library mucosa-associated reveals regions intestine disease.BMC 2011; (561) limitations past include relatively shallow sequencing depth rarely surpasses genus level, small sizes, notwithstanding inherent complexity studying microbiota,9Levy consideration composition, functionality, member interactions, factors. limitations, noted findings indicate composition patient specific, no single suspect UC, supporting notion diverse members progression. evident co-occur merely byproduct difficult investigate. Prospective notoriously challenging conduct. study used samples first-degree relatives collected Colitis Canada's Environmental Microbial project identify CD.18Raygoza Garay J.A. Turpin W. Lee S.-H. al.Gut onset Disease relatives.Gastroenterology. 165: 670-681Abstract (12) Using machine learning, Risk Score was generated 70 who developed (of 3483 total participants), which Ruminococcus torques Blautia (both mucin-degraders), Colidextribacter, Oscillospiraceae, Roseburia predictors onset.18Raygoza In addition, changes, activity, were previously later UC.19Galipeau H.J. Caminero al.Novel biomarkers diagnosis colitis.Gastroenterology. 160: 1532-1545Abstract (86) These pioneering provide stepping stone trace changes before at-risk groups throughout natural progression disease. Such information help transition Many animal demonstrated drive dysbiosis, also inflammation.20Singh V.P. Proctor S.D. Willing B.P. Koch's postulates, disease.Clin Microbiol Infect. 2016; 22: 594-599Abstract (33) 21Glymenaki Singh G. Brass al.Compositional mucus colitis-induced inflammation.Inflamm 23: 912-922Crossref (41) 22Ni Wu G.D. Albenberg L. causation correlation?.Nat 14: 573-584Crossref (971) should exercise caution when extrapolating rodent models applying human disease,23Walter Armet Finlay B.B. al.Establishing exaggerating causality microbiome: lessons microbiota-associated rodents.Cell. 180: 221-232Abstract (271) this positive feedback loop unfortunate "recipe" Even so, reflects array intertwined bacterial-host differs based status, baseline microbiota. One popular hypothesis progression, facilitated concomitant commensals24Cococcioni Panelli Varotto-boccazzi I. al.IBDs pediatric age: peculiarities involvement microbiota.Dig 53: 17-25Scopus (7) metabolites, short-chain fatty acid butyrate.25Byndloss M.X. Olsan E.E. Rivera-Chávez F. al.Microbiota-activated PPAR-g signaling inhibits expansion.Science. 575: 570-575Google Reduced butyrate levels shift colonocyte metabolism phosphorylation glycolysis, elevating luminal oxygen accelerating strict anaerobes.25Byndloss Correspondingly, know facultative anaerobic commensals, coli, survive oxygen-rich environment, assume vacated niches, acquire nutrients, expand numbers.25Byndloss Scholar,26Baldelli V. Scaldaferri Putignani enterobacteriaceae diseases.Microorganisms. 9: 1-15Google Along commensal E there other possessing known "pathobionts" hypothesized either initiation, aggravation IBD.27Chow Tang Mazmanian S.K. Pathobionts gastrointestinal disease.Curr Opin 473-480Crossref (309) term "pathobiont" first introduced 2008 Helicobacter hepaticus, where bacterium potential.28Mazmanian Round J.L. Kasper D.L. A symbiosis prevents 2008; 453: 620-625Crossref (1814) initial definition describe function,29Stecher B. Maier Hardt W.D. "Blooming" gut: how might pathogen evolution.Nat 277-284Crossref (262) 30Ha C.W.Y. Martin Sepich-Poore al.Translocation viable mesenteric adipose drives formation humans.Cell. 183: 666-683Abstract (174) 31Mottawea Chiang C.K. Mühlbauer al.Altered microbiota-host mitochondria crosstalk 713419Google 32Yang Nguyen Khetrapal al.Within-host evolution pathobiont facilitates liver translocation.Nature. 2022; 607: 563-570Crossref (45) "IBD pathobionts" micro-organisms able cause via niche-seeking tendencies. best-characterized adherent-invasive (AIEC). First isolated 1998,33Darfeuille-Michaud Neut Barnich al.Presence strains ileal mucosa disease.Gastroenterology. 1998; 115: 1405-1413Abstract (687) CD, bacteria functions (such invasion) rather markers, meaning express toxins virulence AIEC strain LF82 uses its adhesin FimH adhere cells (IEC) expressing carcinoembryonic antigen-related adhesion molecule 6 receptor.34Dreux Denizot Martinez-Medina al.Point mutations disease-associated enhance response.PLoS Pathog. e1003141Crossref (123) Scholar,35Barnich Carvalho F.A. Glasser A.L. al.CEACAM6 acts receptor colonization disease.J Invest. 117: 1566-1574Crossref (449) Because expression up-regulated explain AIEC's preferential adherence inflammation. Moreover, inside cells, macrophages, triggering release proinflammatory cytokines.36Glasser Boudeau al.Adherent replicate macrophages inducing death.Infect Immun. 69: 5529-5537Crossref (346) Recently invasion, strains, correlate potentiation mice, indeed inflammation.37Kittana Gomes-neto Heck al.Evidence (AIEC) inflammation.mSphere. 8 (e00478-22)Google Recent success blocking identifying targeting prove effective treating symptoms future.38Chevalier Laveissière Desachy al.Blockage disease.Microbiome. 1-16Google instrumental advancing our understanding already described previous articles.39Darfeuille-Michaud Adherent-invasive coli: s pathotype disease.Int Med 2002; 292: 185-193Crossref 40Rolhion Darfeuille-Michaud disease.Inflamm 13: 1277-1283Crossref (210) 41Martinez-Medina Garcia-Gil L.J. chronic diseases: update pathogenicity.World Pathophysiol. 5: 213Crossref 42Palmela Chevarin Xu Z. al.Adherent-invasive disease.Gut. 67: 574-587Crossref (316) 43Mansour Asrar Elhenawy multifaceted coli.Gut Microbes. 152172669Google Instead, focus pathogenesis. Under states perturbation, alter host's state seeking out producing surface structures thus exacerbating By addressing pathologies, underscore playing active development, severity, actions underlie cases failed treatment response frequent relapse. prominent source pathobionts. They individuals44Bücker R. Schulz Günzel al.α-Haemolysin potentiator colon.Gut. 63: 1893-1901Crossref (52) 45Bhattacharjee Flores Woelfel-Monsivais al.Diversity Clostridium innocuum microbiota.mSphere. 46Nadalian Yadegar Houri al.Prevalence meta-analysis.J 36: 852-863Crossref (35) reside causing detectable disease, environment largest determining When becomes perturbed,9Levy disrupted balance commensals support expansion production harmful metabolic byproducts, Inflammation perturbation underlies emergence expansion, similar blooms.9Levy precedes during onset,18Raygoza effects requires investigation. With being arguably important contributing must heritable,47Turpin Goethel Bedrani al.Determinants heritability: genes, bugs, more.Inflamm 24: 1133-1148Crossref (103) factors48Turpin Espin-Garcia O. genome cohort.Nat 48: 1413-1417Crossref (311) through vertical transmission.49Torres Hu Seki al.Infants born mothers altered transfers abnormalities adaptive system germ-free mice.Gut. 42-51Crossref (111) Scholar,50Kim E.S. Tarassishin Eisele al.Longitudinal calprotectin among pregnant women babies.Gastroenterology. 1118-1130.e3Abstract (38) infant strongly influenced maternal microbiome49Torres Scholar,51Wang Ryan Boyaval al.Maternal transmission affecting early-life development.Trends 28: 28-45Abstract (97) diagnosed younger ages, while suffering ever before,24Cococcioni Scholar,52Day Lemberg D.A. Identification colitisin children.J Paediatr Child Health. 56: 1731-1734Google acquisition familial peri-natal 2019 had lower detected infant's stool.49Torres assessing consequences, sourced stool, imbalance systems recipient mice. Cells colonic lamina propria showed reduction class-switched memory B immunoglobulin (Ig) A+ regulatory T (mother's stool only).49Torres Also transmission, elevated infants low experienced life correlation composition.50Kim Extending concepts mouse dam neonate resulted adult mice colonized AIEC.53Brand M.W. Hostetter J.M. al.Vertical attaching . neonatal predisposes following colitic insult life.PLoS One. 17e0266005Google Currently, ongoing trial investigating utero mother newborn determine subsequent (ClinicalTrials.gov Identifier: NCT03116568). heritable, large, carefully controlled humans required if acquired infants, promoting Parental transfer families; therefore, discussions approached until validated interventions available. Another oral microbiome, increasingly recognized contributor pathogenesis, patients.54Schirmer Denson Vlamakis linked course.Cell 2
Язык: Английский
Процитировано
73
Nature Medicine, Год журнала: 2024, Номер 30(3), С. 785 - 796
Опубликована: Фев. 16, 2024
Abstract Multiple clinical trials targeting the gut microbiome are being conducted to optimize treatment outcomes for immune checkpoint blockade (ICB). To improve success of these interventions, understanding changes during ICB is urgently needed. Here through longitudinal profiling 175 patients treated with advanced melanoma, we show that several microbial species-level genome bins (SGBs) and pathways exhibit distinct patterns from baseline in achieving progression-free survival (PFS) 12 months or longer (PFS ≥12) versus PFS shorter than <12). Out 99 SGBs could discriminate between two groups, 20 were differentially abundant only at baseline, while 42 after initiation. We identify five four had consistently higher abundances ≥12 <12 months, respectively. Constructing a log ratio SGBs, find an association overall survival. Finally, different dynamics contexts including type regimen, development immune-related adverse events concomitant medication use. Insights into host factors regimens will be critical guiding rational microbiome-targeted therapies aimed enhancing efficacy.
Язык: Английский
Процитировано
50
Journal Of Clinical Periodontology, Год журнала: 2023, Номер 50(6), С. 736 - 743
Опубликована: Янв. 26, 2023
This Mendelian randomization (MR) study was performed to explore the potential bidirectional causal association between inflammatory bowel disease (IBD) and periodontitis.We used genetic instruments from genome-wide summary statistics of European descent for IBD (12,882 cases 21,770 controls) investigate with periodontitis (3046 195,395 vice versa. The radial inverse-variance weighted method carried out obtain primary estimates, robustness results assessed by a series sensitivity analyses. Due multiple testing, associations p values <.008 were considered as statistically significant, ≥.008 <.05 suggestively significant.In whole associated an increased risk (odds ratio [OR], 1.060; 95% confidence interval [CI], 1.017; 1.105; = .006). Subtype analyses showed that ulcerative colitis (UC) (OR, 1.074; CI 1.029; 1.122; .001), while Crohn's (CD) not. Regarding reverse direction, suggestive 1.065; 1.013; 1.119; .014). revealed CD 1.100; 1.038; 1.167; .001) but not UC. final models after outlier removal no obvious pleiotropy, indicating our analysis reliable.The present MR provides moderate evidence on relationship periodontitis. found in marginal and, possibly, limited clinical relevance. More studies are needed support findings current study.
Язык: Английский
Процитировано
42
Nature Communications, Год журнала: 2024, Номер 15(1)
Опубликована: Янв. 2, 2024
Abstract The sophisticated hierarchical structure that precisely combines contradictory mechanical and biological characteristics is ideal for biomaterials, but it challenging to achieve. Herein, we engineer a spatiotemporally guided bone regeneration (GBR) membrane by rational bilayer integration of densely porous N-halamine functionalized bacterial cellulose nanonetwork facing the gingiva loosely chitosan-hydroxyapatite composite micronetwork alveolar bone. Our GBR asymmetrically combine stiffness flexibility, ingrowth barrier guiding, as well anti-bacteria cell-activation. dense layer has mechanically matched space maintenance capacity toward gingiva, continuously blocks fibroblasts, prevents invasion with multiple mechanisms including release-killing, contact-killing, anti-adhesion, nanopore-blocking; loose ultra-soft conformally cover surfaces defect cavity edges, enables osteogenesis-associated cells, creates favorable osteogenic microenvironment. As result, our all-in-one possesses full protective abilities in GBR.
Язык: Английский
Процитировано
31
Nature Microbiology, Год журнала: 2024, Номер 9(6), С. 1555 - 1565
Опубликована: Май 2, 2024
Язык: Английский
Процитировано
26
Trends in Microbiology, Год журнала: 2024, Номер 32(10), С. 970 - 983
Опубликована: Март 19, 2024
The small intestinal microbiota (SIM) is essential for gastrointestinal health, influencing digestion, immune modulation, and nutrient metabolism. Unlike the colonic microbiota, SIM has been poorly characterized due to sampling challenges ethical considerations. Current evidence suggests that consists of five core genera additional segment-specific taxa. These bacteria closely interact with human host, regulating absorption Recent work presence two forms bacterial overgrowth, one dominated by oral (SIOBO) a second coliform bacteria. Less invasive techniques, omics approaches, mechanistic studies will allow more comprehensive understanding SIM, paving way interventions engineering towards better health.
Язык: Английский
Процитировано
19