Journal of Biological Chemistry, Journal Year: 2024, Volume and Issue: unknown, P. 107771 - 107771
Published: Sept. 1, 2024
Language: Английский
Nature reviews. Cancer, Journal Year: 2022, Volume and Issue: 22(12), P. 703 - 722
Published: Oct. 17, 2022
Language: Английский
Citations
149
Microorganisms, Journal Year: 2022, Volume and Issue: 10(8), P. 1495 - 1495
Published: July 25, 2022
Subacute ruminal acidosis (SARA) is a common metabolic disease in ruminants. In the early stage of SARA, ruminants do not exhibit obvious clinical symptoms. However, SARA often leads to local inflammatory diseases such as laminitis, mastitis, endometritis and hepatitis. The mechanism by which largely unknown. gut microbiota totality bacteria, viruses fungi inhabiting gastrointestinal tract. Studies have found that only crucial health but also involved variety processes, including diseases, autoimmune tumors diseases. shown intestinal bacteria their metabolites can migrate extraintestinal distal organs, lung, liver brain, through endogenous pathways, leading related Combined with literature, we believe dysbiosis rumen microbiota, destruction barrier function pathogenesis lead entry and/or into body blood or lymphatic circulation place "chronic low-grade" state. Meanwhile, mammary gland, uterus other occurrence aim this review describe causes obtain more comprehensive profound understanding its it great significance for joint prevention control
Language: Английский
Citations
49
ACS Chemical Neuroscience, Journal Year: 2023, Volume and Issue: 14(6), P. 1045 - 1062
Published: March 3, 2023
The gut-brain axis (GBA) is the umbrella term to include all bidirectional communication between brain and gastrointestinal (GI) tract in mammalian body. Evidence from over two centuries describes a significant role of GI microbiome health disease states host organism. Short-chain fatty acids (SCFAs), mainly acetate, butyrate, propionate that are physiological forms acetic acid, butyric propionic acid respectively, bacteria derived metabolites. SCFAs have been reported influence cellular function multiple neurodegenerative diseases (NDDs). In addition, inflammation modulating properties make them suitable therapeutic candidates neuroinflammatory conditions. This review provides historical background GBA current knowledge individual central nervous system (CNS) disorders. Recently, few reports also identified effects metabolites case viral infections. Among these viruses, flaviviridae family associated with neuroinflammation deterioration CNS functions. this context, we additionally introduce SCFA based mechanisms different pathogenesis understand former's potential as agents against flaviviral disease.
Language: Английский
Citations
33
Frontiers in Neuroscience, Journal Year: 2023, Volume and Issue: 17
Published: Sept. 28, 2023
Approximately one third of non-hospitalized coronavirus disease 2019 (COVID-19) patients report chronic symptoms after recovering from the acute stage severe respiratory syndrome 2 (SARS-CoV-2) infection. Some most persistent and common complaints this post-acute COVID-19 (PACS) are cognitive in nature, described subjectively as “brain fog” also objectively measured deficits executive function, working memory, attention, processing speed. The mechanisms these sequelae currently not understood. SARS-CoV-2 inflicts damage to cerebral blood vessels intestinal wall by binding angiotensin-converting enzyme (ACE2) receptors evoking production high levels systemic cytokines, compromising brain’s neurovascular unit, degrading barrier, potentially increasing permeability both harmful substances. Such substances hypothesized be produced gut pathogenic microbiota that, given profound effects has on gastrointestinal system, may fourish a result post-COVID-19 dysbiosis. therefore create scenario which neurotoxic neuroinflammatory readily proliferate lumen encounter weakened gaining access brain subsequently producing deficits. Here, we review proposed PACS pathogenesis along gut-brain axis, while identifying specific methodologies that available experimentally measure each individual component model.
Language: Английский
Citations
23
Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13
Published: July 29, 2022
Colorectal cancer (CRC) is one of the leading causes cancer-related death in world. Besides genetic causes, colonic inflammation major risk factors for CRC development, which synergistically regulated by multiple components, including innate and adaptive immune cells, cytokine signaling, microbiota. The complex interaction between gut microbiome has emerged as an important area current research. Metagenomic profiling identified a number prominent CRC-associated bacteria that are enriched patients, linking microbiota composition to colitis development. Some species have been reported promote development preclinical models, while few others modulators induce potent protective immunity against CRC. Mechanistically, regulates activation different cell populations, inflammation, via crosstalk signaling pathways, nuclear factor kappa B (NF-κB), type I interferon, inflammasome. In this review, we provide overview potential interactions host how their could regulate CRC, thus highlighting roles mechanisms microbiota-based therapies prevent or alleviate
Language: Английский
Citations
29
Nature reviews. Cancer, Journal Year: 2023, Volume and Issue: 23(8), P. 565 - 576
Published: June 6, 2023
Language: Английский
Citations
21
Journal of Allergy and Clinical Immunology, Journal Year: 2023, Volume and Issue: 152(2), P. 326 - 337
Published: June 3, 2023
The pervasive role of the innate immune system is established by interferons. Emerging research shows an underappreciated ability macrophages to regulate and propagate interferon responses in infectious autoinflammatory disease states. In this review, we will discuss recent findings demonstrating immunomodulating effects macrophage signaling. Apart from provoking cellular antimicrobial defenses, interferons augment inflammatory activity macrophages. These immunologic adaptations place center at forefront immunity. Consequently, are implicated pathogenesis interferon-driven disorders, such as SLE. these states, recognition immunogenic ligands triggers adopt phenotype through This amplify responses, eventually leading autoinflammation. A better understanding macrophage's signaling support future elucidation novel targets amendable for clinical treatment. Interferons (IFNs) underlie competence ward off pathogens. viral infections, IFNs secreted induce antiviral state host cells, supporting our first line defense against pathogens.1Durbin J.E. Fernandez-Sesma A. Lee C.K. Rao T.D. Frey A.B. Moran T.M. et al.Type I IFN modulates specific immunity.J Immunol. 2000; 164: 4220-4228Crossref PubMed Google Scholar Moreover, recruit leukocytes site infection their activity.2Lee A.J. Ashkar A.A. dual nature type II interferons.Front 2018; 9: 2061Crossref Scopus (343) measures ultimately aim interfere with replication dissemination, curtailing infection. Perturbed may therefore severity susceptibility infections.3Posseme C. Llibre Charbit B. Bondet V. Rouilly Saint-André al.Early IFNβ secretion determines variable downstream IL-12p70 upon TLR4 activation.Cell Rep. 2022; 39110989Abstract Full Text PDF (0) Predictably, impaired a hallmark severe COVID-19 manifestation.4Stertz S. Hale B.G. Interferon deficiencies exacerbating pandemic virus infections.Trends Microbiol. 2021; 29: 973-982Abstract Scholar,5Hadjadj J. Yatim N. Barnabei L. Corneau Boussier Smith al.Impaired patients.Science (1979). 2020; 369: 718-724Crossref More than half century since discovery, now known extend well beyond responses. Namely, orchestrate various distinct homeostatic processes maintain physiological integrity.6Place D.E. Malireddi R.K.S. Kim Vogel P. Yamamoto M. Kanneganti Osteoclast fusion bone loss restricted inducible guanylate binding proteins.Nat Commun. 12: 1-9Crossref (35) Scholar,7Katlinskaya Y.V. Katlinski K.V. Lasri Li Beiting D.P. Durham A.C. control proliferation function intestinal epithelium.Mol Cell Biol. 2016; 36: 1124-1135Crossref (26) Accordingly, disconcerted have long been drive SLE Aicardi-Goutières syndrome. addition, commonly contribute local or systemic inflammation seen rheumatoid arthritis activation Because perturbed appears common denominator conditions, they widely recognized so-called interferonopathies. necessitates investigative efforts into all facets infer clinically relevant reduce burden disease. directed toward interfering microbial principally enhancing interferon-stimulated gene (ISG) expression. On infection, nearly any cell produce intrinsic response microbials, but also protect neighboring cells activate leukocytes. Purposely, some competent producers themselves highly responsive regulatory IFNs, forming feed-forward loop. capacity dependent on lineage microenvironment, like presence pathogens cytokines. Classically, there lineages specialized types IFNs. For instance, plasmacytoid dendritic accepted be predominant III whereas T foremost IFN-secreting leukocytes.8Fitzgerald-Bocarsly Dai Singh Plasmacytoid IFN: 50 years convergent history.Cytokine Growth Factor Rev. 2008; 19: 3Crossref (261) Scholar, 9Psarras Alase Antanaviciute Carr I.M. Md Yusof M.Y. Wittmann al.Functionally non-haematopoietic sources characterize human autoimmunity.Nat 11: 1-18Crossref (10) 10Yin Z. Deng Sheikh F. Natalia Shih T. produced stimulate cells.J 2012; 189: 2735Crossref (137) 11Schoenborn J.R. Wilson C.B. Regulation interferon-gamma during adaptive responses.Adv 2007; 96: 41-101Crossref (1229) However, other IFN-producing identified, including macrophages,12Ali Mann-Nüttel R. Schulze Richter Alferink Scheu Sources immunity: not always driver's seat.Front 2019; 10: 778Crossref (33) 13Darwich Coma G. Peña Bellido Blanco E.J.J. Este J.A. al.Secretion demonstrated single-cell level after costimulation interleukin (IL)-12 plus IL-18.Immunology. 2009; 126: 386-393Crossref (139) 14Bao Y. Liu X. Han Xu Xie Zhang Q. al.Identification IFN-γ-producing B cells.Cell Res. 2013; 24: 161-176Crossref (94) 15Nikonova Khaitov Jackson D.J. Traub Trujillo-Torralbo M.B. Kudlay D.A. al.M1-like potent anti-viral M1-associated marker-positive lung decreased rhinovirus-induced asthma exacerbations.EBioMedicine. 54102734Abstract (13) thereby challenging current dogma lone producers. macrophages, being both tissue-resident derived migratory monocytes, facilitates universal tissue homeostasis immunity.16Zhang Yang Ericsson Function disease: molecular mechanisms.Front 635Google Importantly, effective mediators immunity taking judge, jury, executioner Pathogen receptors (PRRs) constitute wide number sensors use judge environmental exposures, pathogen-associated patterns (PAMPs). main PRRs consider transmembrane Toll-like (TLRs) cytosolic retinoic acid–inducible 1 (RIG-I) melanoma differentiation–associated 5 (MDA5). Macrophages repertoire discriminate between intracellular versus extracellular pathogens, bacterial, endogenous exogenous effectively enabling execute appropriate set actions environment, propagation response. secreting placing them system.1Durbin Scholar,12Ali Yet, central implicates interferonopathies.17Chen H.J. Tas S.W. de Winther M.P.J. Type-I atherosclerosis.J Exp Med. 217e20190459Crossref (39) Scholar,18Moulton V.R. Suarez-Fueyo Meidan E. H. Mizui Tsokos G.C. Pathogenesis lupus erythematosus: perspective.Trends Mol 2017; 23: 615Abstract (241) Transcriptional profiling using state-of-the-art technological advancements has allowed characterization steering system, shedding light delicate cascades. review cover networks underlying An integral feature enhance responsiveness challenges. were observed more ago yet fully elucidated.19Stewart II, W.E. Gosser L.B. Lockart Jr., R.Z. Priming: nonantiviral interferon.J Virol. 1971; 7: 792Crossref Since then, comprise 3 classes cytokines: I, There several subclasses (including IFN-α subtypes IFN-β) (IFN-λ1 4), single (IFN-γ). evolutionary advantage largely unknown, functional differences come down receptor affinity.20Wittling M.C. Cahalan S.R. Levenson E.A. Rabin R.L. Shared unique features interferon-beta interferon-alpha subtypes.Front 3325Crossref (22) Scholar,21Jaks Gavutis Uzé Martal Piehler Differential subunit affinities govern differential signal activation.J 366: 525-539Crossref (166) Despite shared nomenclature, different share little structural homology.22Ealick S.E. Cook W.J. Vijay-Kumar Carson Nagabhushan T.L. Trotta P.P. al.Three-dimensional structure recombinant interferon-γ.Science 1991; 252: 698-702Crossref 23Radhakrishnan Walter L.J. Hruza Reichert al.Zinc mediated dimer 2b revealed X-ray crystallography.Structure. 1996; 4: 1453-1463Abstract 24Karpusas Nolte Benton Meier W. Lipscomb W.N. Goelz crystal beta 2.2-A resolution.Proc Natl Acad Sci U S 1997; 94: 11813-11818Crossref each class binds receptor, canonically eliciting Their commonality role, exerting either autocrine paracrine (Fig 1). Biochemically, IFN-α/β 2 conformational change, allowing tyrosine kinase Janus (JAK) phosphorylate transducer activator transcription (STAT1) (STAT2), causing heterodimerization. STAT1/STAT2 recruits factor 9 (IRF9) assemble heterotrimeric complex IFN-stimulated (ISGF3). Distinctly, IFN-γ 2, JAK1- JAK2-mediated phosphorylation homodimerization STAT1. newly formed translocate nucleus bind gamma-activated sequence promoter elements, ISGF3 elements (ISREs), promoting expression ISGs. Type heterodimeric IFN-λ IL-10 subunit, pathway ISGs located ISREs, mainly encoding proteins properties pathogenic exposures. Some most well-characterized oligoadenylate synthetases, IFN-induced tetratricopeptide repeats, GTP-binding protein. Strikingly, IRFs ISGs, thus generating positive feedback loop Similarly, under ISREs. Altogether work concert, targeting stages life-cycle, entry egress.25Schoggins J.W. Interferon-stimulated genes: what do do?.Annu Rev 6: 567-584Crossref (380) extensively studied given how studying nonviral relatively novel, about antibacterial It likely eradicate bacterial similar way limiting conserved aspects migration.26LeMessurier K.S. Häcker Chi Tuomanen Redecke protects pneumococcal invasive inhibiting transmigration across lung.PLoS Pathog. 9e1003727Crossref (65) 27Helbig K.J. Teh Crosse K.M. Monson Tran E.N. al.The stimulated viperin, restricts Shigella flexneri vitro.Sci 1-12Crossref (15) 28Alphonse Wanford J.J. Voak Gay Venkhaya Burroughs O. al.A family virulence factors dampens blocking calcium signaling.Cell. 185: 2354-2369.e17Abstract 29Kumaran Satyanarayanan El Kebir D. Soboh Butenko Sekheri Saadi al.IFN-β macrophage-derived effector cytokine facilitating resolution inflammation.Nat 3471Crossref (71) monocyte mobilization stimulating chemokines, C-C motif ligand C-X-C chemokine 10.30Lee Chen Chew M.V. Barra N.G. Shenouda M.M. Nham al.Inflammatory monocytes require NK via IL-18 mucosal infection.J 214: 1153Crossref (60) Scholar,31Yarilina Park-Min K.H. Antoniv Hu Ivashkiv TNF activates IRF1-dependent sustained chemokines STAT1-dependent interferon-response genes.Nat 378-387Crossref (328) serve upstream determinants mediating IL-12 monocytes.3Posseme requiring negative regulation anti-inflammatory IL-10.32McNab F.W. Ewbank Howes Moreira-Teixeira Martirosyan Ghilardi induces production IL-27–independent manner blocks killing Mycobacterium tuberculosis–infected macrophages.J 2014; 193: 3600-3612Crossref Interestingly, regulated sensing LPS (a wall component), unleash response, sequentially upregulate IL-10, resolving inflammation.33Ernst Glucksam-Galnoy Bhatta Athamna Ben-Dror I. Glick al.Exclusive temporal stimulation LPS-stimulated mouse cAMP inducers 1788Crossref (18) Scholar,34Ernst Ben-Arosh Levy-Rimler amplifies early MyD88-dependent i interferon-independent LPS-induced interleukin-10 macrophages.Mediators Inflamm. 20193451461Crossref (9) suggest form circuit able reprogram promote resolution. it notorious signature genes containing promotor promotors enhancers Perhaps well-established effect enhancement antigen presentation MHC-II, arm immunity.35Eiz-Vesper Schmetzer H.M. Antigen-presenting cells: potential proven new players therapies.Transf Med Hemother. 47: 429-431Crossref (14) supports clearance microbials boosting core macrophage, phagocytosis cytokines, nitric oxide, reactive oxygen species.36Kak Raza Tiwari B.K. Interferon-gamma (IFN-γ): exploring its implications diseases.Biomol Concepts. 64-79Crossref (248) significance differentiate even absence M-CSF.37Luque-Martin Angell D.C. Kalxdorf Bernard Thompson Eberl H.C. al.IFN-γ drives differentiation proinflammatory that resemble psoriasis.J 207: 555-568Crossref (8) Thereby, pathways distinct. Still, shown overlap. partially explained STAT1 homodimers, ISGF3,38Mazewski Perez R.E. Fish Platanias L.C. (IFN)-regulated canonical non-canonical pathways.Front 3025Crossref (56) 39Kok Rosenblatt Teusel Nizharadze Magalhães V.G. Dächert al.Disentangling mechanisms regulating sensitization alpha transduction.Mol Syst 16: e8955Crossref (5) 40Platanitis Demiroz Schneller Fischer K. Capelle Hartl switch STAT2-IRF9 underlies interferon-induced transcription.Nat 1-17Crossref (85) tread substantial overlap especially apparent lacking STAT2 IRF9, disabling formation ISGF3.41Gothe Stremenova Spegarova Hatton C.F. Griffin Sargent Cowley S.A. al.Aberrant IRF9 deficiency.J Allergy Clin 150: 955-964.e16Abstract When disrupted, show associated stimulation. As discovered 2003, addition system.42Galani I.E. Triantafyllia Eleminiadou E.E. Koltsida Stavropoulos Manioudaki al.Interferon-λ mediates non-redundant front-line protection influenza without compromising fitness.Immunity. 46: 875-890.e6Abstract (290) Scholar,43Kotenko S.V. Gallagher Baurin V.V. Lewis-Antes Shen Shah N.K. al.IFN-lambdas mediate complex.Nat 2003; 69-77Crossref (1554) Investigative additive value over rudimentary featuring only Current leads tissue-specific first-responder strong response.42Galani Scholar,44Contoli Message S.D. Laza-Stanca Edwards M.R. Wark P.A.B. 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Besides myeloid-lineage homeostasis. pivotal osteoclast homeostasis, where signals involved osteoclastogenesis.6Place because reduced density.56Duque Dion MacOritto Rivas al.Interferon-γ plays vivo rescues osteoporosis ovariectomized Bone Miner 2011; 26: 1472-1483Crossref Scholar,57Salem Gao Wang Nguyen-Yamamoto Goltzman (IRF1) metabolism.J 18: 1588-1598Crossref (20) Of particular interest, density diseases, arthritis58Bultink I.E.M. connective disease/systemic erythematosus.Calcif Tissue Int. 102: 575-591Crossref Scholar,59Llorente García-Castañeda Valero González-Álvaro Castañeda Osteoporosis arthritis: dangerous liaisons.Front (Lausanne). 802Google Scholar; possibly adding 65 ago, mammalian characterized possess inherent exposures.60Isaacs Lindenmann Virus interference, I: 1957; 429-438Crossref Moving forward, plethora types, roles, discovered.42Galani 875-890.e6Abs
Language: Английский
Citations
19
The Journal of Experimental Medicine, Journal Year: 2023, Volume and Issue: 221(1)
Published: Dec. 12, 2023
Type I interferons (IFNs) exert a broad range of biological effects important in coordinating immune responses, which have classically been studied the context pathogen clearance. Yet, whether immunomodulatory bacteria operate through IFN pathways to support intestinal tolerance remains elusive. Here, we reveal that commensal bacterium, Bacteroides fragilis, utilizes canonical antiviral modulate dendritic cells (DCs) and regulatory T cell (Treg) responses. Specifically, signaling is required for commensal-induced as IFNAR1-deficient DCs display blunted IL-10 IL-27 production response B. fragilis. We further establish IFN-driven critical shaping ensuing Foxp3+ Treg via IL-27Rα signaling. Consistent with these findings, single-cell RNA sequencing gut Tregs demonstrated colonization fragilis promotes distinct gene signature during inflammation. Altogether, our findings demonstrate role commensal-mediated tonic type
Language: Английский
Citations
19
Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 160, P. 114414 - 114414
Published: Feb. 20, 2023
Microbiota-derived short-chain fatty acids (SCFAs) are crucial for protecting the intestinal barrier and regulating immune response during infections. Recent studies show that viral infections alter local microbiota SCFA synthesis, there is mounting evidence linking low levels in individuals with an increased risk of contracting Based on type virus, SCFAs may have either antiviral or pro-viral activity. Butyrate, instance, prevents tissue injury caused by neutrophil infiltration into airways, which occurs when mice infected influenza. Bone marrow-derived free acid receptor 3 (FFAR3) induced butyrate leads to conversion monocytes alternatively activated macrophages (AAMs) instead proinflammatory macrophages, turn reduces recruitment lung. Treatment CD8 + T cell responsiveness influenza virus enhancing their metabolism functional In addition, control interferon (IFN) responses diseases. acetate inhibit respiratory syncytial (RSV) boosting IFN-β a G-protein-coupled 43 (GPR43)-dependent way. Injection SCFA-producing Lachnospiraceae exogenous RSV pulmonary load, inflammatory cells lung, increases animal survival. It has been shown propionate both provide comparable safeguards. Increased NF-kappa B (NF-kB) p65 translocation nucleus administration provides scientific proof NF-kB activation implicated connection between GPR43 interaction production; however, this mechanism requires additional investigations. article, we will critically analyze function various infections, discussing summarizing many impacts action mechanisms SCFAs.
Language: Английский
Citations
18
World Journal of Gastroenterology, Journal Year: 2024, Volume and Issue: 30(10), P. 1295 - 1312
Published: March 14, 2024
Hepatitis B virus (HBV) reactivation is a clinically significant challenge in disease management. This review explores the immunological mechanisms underlying HBV reactivation, emphasizing progression and It delves into host immune responses reactivation’s delicate balance, spanning innate adaptive immunity. Viral factors’ disruption of this as are interactions between viral antigens, cells, cytokine networks, checkpoint pathways, examined. Notably, roles T natural killer antigen-presenting cells discussed, highlighting their influence on progression. impact severity, hepatic flares, liver fibrosis progression, hepatocellular carcinoma detailed. Management strategies, including anti-viral immunomodulatory approaches, critically analyzed. The role prophylactic therapy during immunosuppressive treatments explored alongside novel immunotherapeutic interventions to restore control prevent reactivation. In conclusion, comprehensive furnishes holistic view that propel With dedicated focus understanding its implications for prospects efficient management article contributes significantly knowledge base. more profound insights intricate elements system will inform evidence-based ultimately enhancing elevating patient outcomes. dynamic landscape strategies scrutinized, approaches. preventing potential innovative proactively deter
Language: Английский
Citations
8