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• W1529503573 abstract "Links between the human microbiome and the innate and adaptive immune systems and their impact on autoimmune and inflammatory diseases are only beginning to be recognized. Characterization of the complex human microbial community is facilitated by culture-independent nucleic acid sequencing tools and bioinformatics systems. Specific organisms and microbial antigens are linked with initiation of innate immune responses that, depending on the context, may be associated with tolerogenic or effector immune responses. Further complexity is introduced by preclinical data that demonstrate the impacts of dietary manipulation on the prevention of genetically determined, systemic autoimmune disorders and on gastrointestinal microbiota. Investigation of interactions of complex microbial populations with the human immune system may provide new targets for clinical management in allotransplantation. Links between the human microbiome and the innate and adaptive immune systems and their impact on autoimmune and inflammatory diseases are only beginning to be recognized. Characterization of the complex human microbial community is facilitated by culture-independent nucleic acid sequencing tools and bioinformatics systems. Specific organisms and microbial antigens are linked with initiation of innate immune responses that, depending on the context, may be associated with tolerogenic or effector immune responses. Further complexity is introduced by preclinical data that demonstrate the impacts of dietary manipulation on the prevention of genetically determined, systemic autoimmune disorders and on gastrointestinal microbiota. Investigation of interactions of complex microbial populations with the human immune system may provide new targets for clinical management in allotransplantation. Microorganisms in tissues and on barrier surfaces, including chronic colonization and acute infectious shifts, are collectively termed the “microbiome.” Specific organisms differ between individuals, in different anatomic sites and under different clinical conditions (1.Alegre ML Mannon RB Mannon PJ The microbiota, the immune system and the allograft.Am J Transplant. 2014; 14: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 2.Huffnagle GB Noverr MC The emerging world of the fungal microbiome.Trends Microbiol. 2013; 21: 334-341Abstract Full Text Full Text PDF PubMed Scopus (373) Google Scholar, 3.Taur Y Xavier JB Lipuma L Intestinal domination and the risk of bacteremia in patients undergoing allogeneic hematopoietic stem cell transplantation.Clin Infect Dis. 2012; 55 (et al): 905-914Crossref PubMed Scopus (647) Google Scholar, 4.Virgin HW The virome in mammalian physiology and disease.Cell. 2014; 157: 142-150Abstract Full Text Full Text PDF PubMed Scopus (420) Google Scholar, 5.Eckburg PB Diversity of the human intestinal microbial flora.Science. 2005; 308: 1635-1638Crossref PubMed Scopus (5783) Google Scholar). The gut microbiome includes approximately 1014 bacteria, fungi, and viruses. The composition of the microbiome is influenced by diet, microbial exposures, immune status, and genetics (6.Blaser MJ Who are we? Indigenous microbes and the ecology of human diseases.EMBO Rep. 2006; 7: 956-960Crossref PubMed Scopus (222) Google Scholar, 7.Ley R Evolution of mammals and their gut microbes.Science. 2008; 320: 1647-1651Crossref PubMed Scopus (2532) Google Scholar, 8.Zoetendal EG The host genotype affects the bacterial community in the human gastrointestinal tract.Microb Ecol Health Dis. 2001; 13: 129-134Crossref Scopus (461) Google Scholar). Many organisms of the human microbiome are unknown and many are difficult to cultivate in vitro. Culture-independent nucleic acid sequencing tools and bioinformatics systems have allowed study of the microbiota including 16S ribosomal RNA (rRNA) bacterial genomic sequencing and fingerprinting methods (18S for fungi) to assess the relative abundance of species in a sample, and “shotgun” metagenomic sequencing to study viral sequences and structural and metabolic pathways (9.Cox MJ Cookson WO Moffatt MF Sequencing the human microbiome in health and disease.Hum Mol Genet. 2013; 22: R88-R94Crossref PubMed Scopus (99) Google Scholar). Links between the human microbiome, the innate and adaptive immune systems, and their impact on alloimmunity, and autoimmune and inflammatory diseases are beginning to be recognized. The complex and dynamic interface between the human microbiome and the immune system is incompletely described, but best characterized in the gastrointestinal (GI) tract (1.Alegre ML Mannon RB Mannon PJ The microbiota, the immune system and the allograft.Am J Transplant. 2014; 14: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 10.Belkaid Y Hand TW Role of the microbiota in immunity and inflammation.Cell. 2014; 157: 121-141Abstract Full Text Full Text PDF PubMed Scopus (2793) Google Scholar, 11.Alegre ML Bromberg JS Commensal microbiota determine intestinal iTreg.Am J Transplant. 2012; 12: 1967Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar). Under normal conditions, the immense array of microbes that is resident continuously within the GI tract differs between individuals and is sequestered by the mucus layer, antibodies (IgA) and antimicrobial peptides near the mucosal barrier (12.Hill DA Artis D Intestinal bacteria and the regulation of immune cell homeostasis.Annu Rev Immunol. 2010; 28: 623-667Crossref PubMed Scopus (441) Google Scholar, 13.Johansson ME Sjovall H Hansson GC The gastrointestinal mucus system in health and disease.Nat Rev Gastroenterol Hepatol. 2013; 10: 352-361Crossref PubMed Scopus (870) Google Scholar). Developmentally, the immune system evolves in parallel with commensal organisms in the gut to ensure that the host remains tolerant to these “normal” organisms (10.Belkaid Y Hand TW Role of the microbiota in immunity and inflammation.Cell. 2014; 157: 121-141Abstract Full Text Full Text PDF PubMed Scopus (2793) Google Scholar, 14.Olszak T An D Zeissig S Microbial exposure during early life has persistent effects on natural killer T cell function.Science. 2012; 336 (et al): 489-493Crossref PubMed Scopus (1229) Google Scholar, 15.Collado MC Cernada M Bauerl C Vento M Perez-Martinez G Microbial ecology and host-microbiota interactions during early life stages.Gut Microb. 2012; 3: 352-365Crossref PubMed Scopus (182) Google Scholar). Some microbial antigens (Ags) escape across the mucosal barrier and some new organisms, potential pathogens, are introduced. Thus, in the small intestine, bacterial and fungal Ags may traverse the barrier via pores near goblet cells or may be acquired by dendritic cells (DCs) via extensions protruding into the intestinal lumen, or actively transported by microfold (M) cells in Peyer’s patches that acquire Ag directly from the lumen and deliver it to Ag-presenting cells (APCs) to initiate immune responses. The role of gut microorganisms or their products in triggering APCs and initiating alloimmune reactivity is supported by observations in pediatric allogeneic bone marrow transplantation (HSCT) where total GI decontamination of allograft recipients largely prevents acute graft-versus-host disease (GVHD) (12.Hill DA Artis D Intestinal bacteria and the regulation of immune cell homeostasis.Annu Rev Immunol. 2010; 28: 623-667Crossref PubMed Scopus (441) Google Scholar, 16.Vossen JM Guiot HF Lankester AC Complete suppression of the gut microbiome prevents acute graft-versus-host disease following allogeneic bone marrow transplantation.PLoS ONE. 2014; 9 (et al): e105706Crossref PubMed Scopus (78) Google Scholar, 17.Franchi L Kamada N Nakamura Y NLRC4-driven production of IL-1beta discriminates between pathogenic and commensal bacteria and promotes host intestinal defense.Nat Immunol. 2012; 13 (et al): 449-456Crossref PubMed Scopus (306) Google Scholar). In adults undergoing HSCT, maintenance of the pattern of the microbial flora appears to be as important as the specific organisms detected in the prevention of GVHD (3.Taur Y Xavier JB Lipuma L Intestinal domination and the risk of bacteremia in patients undergoing allogeneic hematopoietic stem cell transplantation.Clin Infect Dis. 2012; 55 (et al): 905-914Crossref PubMed Scopus (647) Google Scholar, 18.Holler E Butzhammer P Schmid K Metagenomic analysis of the stool microbiome in patients receiving allogeneic SCT: Loss of diversity is associated with use of systemic antibiotics and more pronounced in gastrointestinal GvHD.Biol Blood Marrow Transplant. 2014; 20 (et al doi: 10.1016/j.bbmt.2014.01.030): 640-645Abstract Full Text Full Text PDF PubMed Scopus (366) Google Scholar). GVHD may also injure Paneth cells and favor replacement of commensals by potential pathogenic organisms (19.Eriguchi Y Takashima S Oka H Graft-versus-host disease disrupts intestinal microbial ecology by inhibiting Paneth cell production of alpha-defensins.Blood. 2012; 120 (et al): 223-231Crossref PubMed Scopus (244) Google Scholar). The complex interplay between inflammatory conditions of the gut and the microbiota merits further investigation. There is evidence that in immune-mediated chronic inflammatory disorders including in murine models of diabetes and autoimmune arthritis, the gut microbiome can protect against as well as exacerbate disease (20.Wen L Ley RE Volchkov PY Innate immunity and intestinal microbiota in the development of Type 1 diabetes.Nature. 2008; 455 (et al): 1109-1113Crossref PubMed Scopus (1548) Google Scholar,21.Abdollahi-Roodsaz S Joosten LA Koenders MI Stimulation of TLR2 and TLR4 differentially skews the balance of T cells in a mouse model of arthritis.J Clin Invest. 2008; 118 (et al): 205-216Crossref PubMed Scopus (417) Google Scholar). Recent studies of host T cell interactions with commensal bacteria have revealed that, in contrast with the paradigm that the immune system is tolerant to gut microbial Ags, gut microbial homeostasis contributes to the maintenance of regulatory and effector T cell responses (22.Nutsch KM Hsieh CS T cell tolerance and immunity to commensal bacteria.Curr Opin Immunol. 2012; 24: 385-391Crossref PubMed Scopus (77) Google Scholar). For example, some commensals (e.g. Clostridia sp.) or patterns of commensals, induce the peripheral differentiation of regulatory T cells (Treg) and tolerance, whereas others, via Toll-like receptor (TLR)2 ligation (e.g. Bacteroides fragilis polysaccharide A), expand preexisting Treg and promote the production of anti-inflammatory IL-10, without which autoimmune inflammatory colitis or encephalitis occurs (23.Mazmanian SK Round JL Kasper DL A microbial symbiosis factor prevents intestinal inflammatory disease.Nature. 2008; 453: 620-625Crossref PubMed Scopus (1752) Google Scholar,24.Wang Y Telesford KM Ochoa-Repáraz J An intestinal commensal symbiosis factor controls neuroinflammation via TLR2-mediated CD39 signalling.Nat Commun. 2014; 5 (et al doi: 10.1038/ncomms5432): 4432Crossref PubMed Scopus (155) Google Scholar). Other commensals or pathogens elicit effector T cell responses and immunity. Further, gram positive segmented filamentous bacteria (SFB), or the TLR5 ligand flagellin appear to skew T cell development toward T helper (Th)17 and Th1 effector cells to enhance inflammation in spontaneous colitis models (25.Goto Y Panea C Nakato G Segmented filamentous bacteria antigens presented by intestinal dendritic cells drive mucosal Th17 cell differentiation.Immunity. 2014; 40 (et al): 594-607Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar,26.Ivanov II Atarashi K Manel N Induction of intestinal Th17 cells by segmented filamentous bacteria.Cell. 2009; 139 (et al): 485-498Abstract Full Text Full Text PDF PubMed Scopus (3324) Google Scholar). SFB are increased in IgA deficiency (27.Suzuki K Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut.Proc Natl Acad Sci USA. 2004; 101: 1981-1986Crossref PubMed Scopus (553) Google Scholar). The effect of SFB on reduction in Treg frequencies in Th17-mediated autoimmune arthritis is reversed by anti-Gram positive antimicrobial therapy (28.Wu HJ Ivanov II Darce J Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells.Immunity. 2010; 32 (et al): 815-827Abstract Full Text Full Text PDF PubMed Scopus (1213) Google Scholar). The data indicate that specific organisms or microbial products and a stable microbiome and the resulting balance between protective responses (tolerant vs. effector) appears to be essential for “normal” gut homeostasis and prevention of immune dysregulation. Previously primed Ag-specific Treg would be envisaged to protect against responses to commensal organisms and to self Ags and migrate systemically to downregulate inflammatory responses induced by APCs, including DCs, macrophages, NK cells and B cells and prevent autoimmune injury. This protective effect may be achieved via secreted cytokines (e.g. IL-10, TGF-β, TNF-α), CTLA4 ligation, T cell-mediated killing of APCs or other mechanisms. How might such tolerance be broken? Multiple models exist in which immune tolerance to transplanted organs is abrogated by inflammatory stimuli, including bacteria (e.g. Staphylococcus aureus, Listeria monocytogenes) and viruses (e.g. cytomegalovirus, lymphocytic choriomeningitis virus) (29.Ahmed EB Wang T Daniels M Alegre ML Chong AS IL-6 induced by Staphylococcus aureus infection prevents the induction of skin allograft acceptance in mice.Am J Transplant. 2011; 11: 936-946Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar, 30.Wang T Chen L Ahmed E Prevention of allograft tolerance by bacterial infection with Listeria monocytogenes.J Immunol. 2008; 180 (et al): 5991-5999Crossref PubMed Scopus (74) Google Scholar, 31.Williams MA Onami TM Adams AB Cutting edge: Persistent viral infection prevents tolerance induction and escapes immune control following CD28/CD40 blockade-based regimen.J Immunol. 2002; 169 (et al): 5387-5391Crossref PubMed Scopus (89) Google Scholar, 32.Cook CH Bickerstaff AA Wang JJ Disruption of murine cardiac allograft acceptance by latent cytomegalovirus.Am J Transplant. 2009; 9 (et al): 42-53Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar). These infections appear to stimulate innate immune mechanisms (DCs, monocytes) that induce either alloreactive (heterologous immunity via cross-reacting epitopes) or preexisting T cell immunity (nonspecific inflammation). It is reasonable to propose that other inflammatory stimuli (ischemia-reperfusion injury, graft rejection, GVHD, infections) may shift the balance from regulatory to effector immune responses. This loss of immune homeostasis may be ascribed to the overwhelming of Treg function by bacterial products that elicit a “cytokine storm,” by specific cytokine release (e.g. IL-1β with autoantibody production) and/or by offsetting the balance between effector and regulatory cells. In these studies certain cytokines were a prerequisite for the observed effects; when IL-6 was elevated, Th17 cells were produced, whereas with low IL-6, Tregs were favored (25.Goto Y Panea C Nakato G Segmented filamentous bacteria antigens presented by intestinal dendritic cells drive mucosal Th17 cell differentiation.Immunity. 2014; 40 (et al): 594-607Abstract Full Text Full Text PDF PubMed Scopus (327) Google Scholar,26.Ivanov II Atarashi K Manel N Induction of intestinal Th17 cells by segmented filamentous bacteria.Cell. 2009; 139 (et al): 485-498Abstract Full Text Full Text PDF PubMed Scopus (3324) Google Scholar,29.Ahmed EB Wang T Daniels M Alegre ML Chong AS IL-6 induced by Staphylococcus aureus infection prevents the induction of skin allograft acceptance in mice.Am J Transplant. 2011; 11: 936-946Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar,30.Wang T Chen L Ahmed E Prevention of allograft tolerance by bacterial infection with Listeria monocytogenes.J Immunol. 2008; 180 (et al): 5991-5999Crossref PubMed Scopus (74) Google Scholar). Nutritional changes, like antimicrobial therapies, appear to impact both the intestinal microbiota and local and systemic immune responses that contribute to autoimmune colitis or arthritis. Diet has a major impact on the maintenance of the GI microbiota and on the availability of metabolites required for function of immune cells (33.Ley RE Turnbaugh PJ Klein S Gordon JI Microbial ecology: Human gut microbes associated with obesity.Nature. 2006; 444: 1022-1023Crossref PubMed Scopus (6461) Google Scholar, 34.Li Y Innocentin S Withers DR Exogenous stimuli maintain intraepithelial lymphocytes via aryl hydrocarbon receptor activation.Cell. 2011; 147 (et al): 629-640Abstract Full Text Full Text PDF PubMed Scopus (601) Google Scholar, 35.Savy M Edmond K Fine PE Landscape analysis of interactions between nutrition and vaccine responses in children.J Nutrition. 2009; 139 (et al): 2154S-2218SCrossref PubMed Scopus (109) Google Scholar, 36.Mora JR Iwata M von Andrian UH Vitamin effects on the immune system: Vitamins A and D take centre stage.Nat Rev Immunol. 2008; 8: 685-698Crossref PubMed Scopus (1150) Google Scholar, 37.Minot S Sinha R Chen J The human gut virome: Inter-individual variation and dynamic response to diet.Genome Res. 2011; 21 (et al): 1616-1625Crossref PubMed Scopus (665) Google Scholar, 38.Zentek J Ferrara F Pieper R Tedin L Meyer W Vahjen W Effects of dietary combinations of organic acids and medium chain fatty acids on the gastrointestinal microbial ecology and bacterial metabolites in the digestive tract of weaning piglets.J Anim Sci. 2013; 91: 3200-3210Crossref PubMed Scopus (98) Google Scholar). For example, retinoic acid is a metabolite of vitamin A that is required for Th17 development, lymphocyte migration and DC maturation (39.Cha HR Chang SY Chang JH Downregulation of Th17 cells in the small intestine by disruption of gut flora in the absence of retinoic acid.J Immunol. 2010; 184 (et al): 6799-6806Crossref PubMed Scopus (132) Google Scholar, 40.Chang SY Cha HR Chang JH Lack of retinoic acid leads to increased langerin-expressing dendritic cells in gut-associated lymphoid tissues.Gastroenterology. 2010; 138 (et al 1478. e1–1478.e6.): 1468-1478Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar, 41.Hall JA Grainger JR Spencer SP Belkaid Y The role of retinoic acid in tolerance and immunity.Immunity. 2011; 35: 13-22Abstract Full Text Full Text PDF PubMed Scopus (399) Google Scholar). Colitis has been reduced in murine models through administration of a high-fat diet (33.Ley RE Turnbaugh PJ Klein S Gordon JI Microbial ecology: Human gut microbes associated with obesity.Nature. 2006; 444: 1022-1023Crossref PubMed Scopus (6461) Google Scholar,42.Gregor MF Hotamisligil GS Inflammatory mechanisms in obesity.Annu Rev Immunol. 2011; 29: 415-445Crossref PubMed Scopus (2626) Google Scholar,43.Devkota S Wang Y Musch MW Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice.Nature. 2012; 487 (et al): 104-108Crossref PubMed Scopus (1293) Google Scholar). Recent studies of Lukens et al (44.Lukens JR Gurung P Vogel P Dietary modulation of the microbiome affects autoinflammatory disease.Nature. 2014; 516 (et al doi: 10.1038/nature13788): 246-249Crossref PubMed Scopus (219) Google Scholar) address this relationship between diet and autoinflammatory disorders by examining Pstip2cmo mice. These animals spontaneously develop osteomyelitis that resembles chronic recurrent multifocal osteomyelitis in humans. IL-1β-mediated mechanisms appear to be important in the development of this disease. In arthritic Pstip2cmo mice fed normal diets, the bacterium Prevotella was found to be prominent in the colonic microbiome. Mice fed diets rich in fat and cholesterol were protected against inflammatory bone disease and bone erosion and also had reductions in intestinal Prevotella levels. These nonarthritic mice also displayed reduced pro-IL-1β systemically in neutrophils (44.Lukens JR Gurung P Vogel P Dietary modulation of the microbiome affects autoinflammatory disease.Nature. 2014; 516 (et al doi: 10.1038/nature13788): 246-249Crossref PubMed Scopus (219) Google Scholar). A reduction in pro-IL-1β expression was also observed with antimicrobial treatment and in wild-type mice kept under germ-free conditions. These observations confirm the role of dietary manipulation in the makeup of the GI microbiome and in protection against genetically determined susceptibilities to autoimmune disease. Thus, environmental changes, including dietary changes or selective antimicrobial treatments affecting the microbiome, may be an important avenue for therapeutic exploration in autoimmune disease and other systemic immune processes including allograft rejection (45.Lu H He J Wu Z Assessment of microbiome variation during the perioperative period in liver transplant patients: A retrospective analysis.Microb Ecol. 2013; 65 (et al): 781-791Crossref PubMed Scopus (61) Google Scholar). Although our comprehension of the relationship between the microbiome and the immune system is still at a very early stage, these recent studies suggest that it may be possible to develop preventive or therapeutic approaches to inflammatory diseases by targeting this axis. Thus, insights into the mechanisms underlying the impact of individual microbes, microbial communities and their byproducts on the relative proportions of effector T cells or Treg in the gut may aid in the design of therapies to reduce alloimmune responses and graft injury or to promote allograft tolerance. Moreover, genetic characterization of the intestinal microbial profile may have utility in identifying those individuals at greater risk for organ rejection and could become a therapeutic target to improve allograft outcomes (46.Ren Z Jiang J Lu H Intestinal microbial variation may predict early acute rejection after liver transplantation in rats.Transplantation. 2014; 98 (et al): 844-852Crossref PubMed Scopus (67) Google Scholar, 47.Lee JR Muthukumar T Dadhania D Gut microbial community structure and complications after kidney transplantation: A pilot study.Transplantation. 2014; 98 (et al): 697-705Crossref PubMed Scopus (124) Google Scholar, 48.Lee JR Dadhania D August P Lee JB Suthanthiran M Muthukumar T Circulating levels of 25-hydroxyvitamin D and acute cellular rejection in kidney allograft recipients.Transplantation. 2014; 98: 292-299Crossref PubMed Scopus (45) Google Scholar). While fecal microbiota transplantation (FMT) may allow restoration of the normal constituents of the microbiome and offer potential for therapy of inflammatory bowel disease, it may be important to identify particular groups of microorganisms for specific disease indications and to develop simpler modes for administration for the “ideal” microbial transplants (49.Pamer EG Fecal microbiota transplantation: Effectiveness, complexities, and lingering concerns.Mucosal Immunol. 2014; 7: 210-214Crossref PubMed Scopus (83) Google Scholar). The risks associated with fecal, probiotic and dietary manipulation merit careful consideration. The impact of such therapies on graft outcomes remain to be ascertained but offers exciting opportunities for future investigation. The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation." @default.
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• W1529503573 title "Clinical Implications of Basic Science Discoveries: Immune Homeostasis and the Microbiome—Dietary and Therapeutic Modulation and Implications for Transplantation" @default.
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