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Host-Microbiota Interactions Shape Local and Systemic Inflammatory Diseases John B Host-Microbiota Interactions Shape Local and Systemic Inflammatory Diseases John B. Grigg and Gregory F. Sonnenberg This information is current as J Immunol 2017; 198:564-571; ; of September 28, 2021. doi: 10.4049/jimmunol.1601621 http://www.jimmunol.org/content/198/2/564 Downloaded from References This article cites 122 articles, 28 of which you can access for free at: http://www.jimmunol.org/content/198/2/564.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 28, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2017 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Th eJournal of Brief Reviews Immunology Host-Microbiota Interactions Shape Local and Systemic Inflammatory Diseases John B. Grigg and Gregory F. Sonnenberg Recent advances in understanding how the mammalian with the microbiota to maintain a state of homeostasis that is immune system and intestinal microbiota functionally mutually beneficial. For example, the requirement for micro- interact have yielded novel insights for human health biota in the proper development of the immune system was first and disease. Modern technologies to quantitatively mea- demonstrated in animals reared in microorganism-free envi- sure specific members and functional characteristics ronments, known as germ-free. Germ-free animals display a of the microbiota in the gastrointestinal tract, along variety of intestinal immune defects, including impaired de- velopment of GALTs, lower amounts of secreted Ig, and re- with fundamental and emerging concepts in the field + of immunology, have revealed numerous ways in which duced intraepithelial CD8 T cells (5). Additionally, evidence Downloaded from host-microbiota interactions proceed beneficially, neu- has supported the notion of the gut microbiota having a strong influence over the development of the immune system outside trally, or detrimentally for mammalian hosts. It is clear + that the gut microbiota has a strong influence on the shape of the intestine (6). In germ-free mice, splenic CD4 Th cells are skewed toward the Th2 cell subset and promote enhanced and quality of the immune system; correspondingly, the allergic responses and type 2 immunity (6). Germ-free mice immune system guides the composition and localization of + also have decreased total numbers of peripheral CD4 Tcells, http://www.jimmunol.org/ the microbiota. In the following review, we examine the including Th17 cells (7) and regulatory T cell (Treg) com- evidence that these interactions encompass homeostasis partments (8, 9). Conversely, the intestinal immune system also and inflammation in the intestine and, in certain cases, actively shapes the composition and compartmentalization of extraintestinal tissues. Lastly, we discuss translational ther- the microbiota through various mechanisms (10–13). Overall, apies stemming from research on host-microbiota interac- these observations demonstrate that the colonizing microbiota tions that could be used for the treatment of chronic and host immune system have a complex, dynamic, and re- inflammatory diseases. The Journal of Immunology, ciprocal dialogue. 2017, 198: 564–571. Members of the microbiota are recognized by the innate im- by guest on September 28, 2021 mune system through their conserved pathogen-associated mo- he human body hosts a remarkable variety (1) and lecular patterns, referred to in this article as microbe-associated quantity (2) of microorganisms collectively referred molecular patterns (MAMPs) (14), to encompass such ligands in T to as the microbiota. The microbiota encompasses Ar- normally nonpathogenic organisms of the microbiota. MAMPs chaea, Bacteria, Eukarya, and viruses that form a complex eco- are recognized by germline-encoded pattern recognition recep- system thought to have coevolved with mammalian hosts over tors distributed spatiotemporally across various cell types and time. Commensal bacteria are the most well-defined member of tissues. Despite this ability to directly respond to microbiota- the microbiota. Among the various body surfaces where com- derived signals, several features of the immune system act in mensal bacteria reside, the gastrointestinal (GI) tract contains the cooperation with the intestinal barrier to protect the body from highest densities, which are estimated to range between 1011 and opportunistic pathogens and to limit the immune system from 1014 cells per gram of luminal content (3). This enormous overreacting to beneficial microbiota in the gut (Fig. 1A). Such cellular and genetic component of the human body is now well features include the following: a thick mucus lining the lumen recognized to provide indispensible functions in digestion, nu- of the gut epithelial cells that physically excludes most micro- trition status, and protection against invasive pathogens (4). organisms (15), secreted IgA that recognizes and binds microbe- The mammalian immune system is also significantly specific epitopes and facilitates their removal (16), and secreted enriched in the GI tract and engages in a complex dialogue antimicrobial peptides that directly neutralize microorganisms Gastroenterology and Hepatology Division, Joan and Sanford I. Weill Department of Address correspondence and reprint requests to Dr. Gregory F. Sonnenberg, Weill Medicine, Weill Cornell Medicine, New York, NY 10021; Department of Microbiology Cornell Medical College, New York, NY 10021. E-mail address: gfsonnenberg@med. and Immunology, Weill Cornell Medicine, New York, NY 10065; and The Jill Roberts cornell.edu Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, New Abbreviations used in this article: AhR, aryl hydrocarbon receptor; CD, Crohn’s disease; York, NY 10021 EAE, experimental autoimmune encephalitis; FMT, fecal microbiota transplant therapy; Received for publication September 19, 2016. Accepted for publication October 31, GI, gastrointestinal; IBD, inflammatory bowel disease; IEC, intestinal epithelial cell; 2016. ILC, innate lymphoid cell; ILC3, group 3 ILC; MAMP, microbe-associated molecular pattern; PSA, polysaccharide A; RA, rheumatoid arthritis; SCFA, short-chain fatty acid; This work was supported by National Institutes of Health Grants DP5OD012116, SFB, segmented filamentous bacteria; Treg, regulatory T cell; WT, wild-type. R01AI123368, R21DK110262, and U01AI095608, the National Institute of Allergy and Infectious Diseases Mucosal Immunology Studies Team, the Crohn’s and Colitis Ó Foundation of America, the Searle Scholars Program, and an American Asthma Foun- Copyright 2017 by The American Association of Immunologists, Inc. 0022-1767/17/$30.00 dation Scholar Award. www.jimmunol.org/cgi/doi/10.4049/jimmunol.1601621 The Journal of Immunology 565 (17, 18). In addition to their pathogen-protective effects, these phenocopy aspects of human disease when experimentally features help to maintain sequestration of the microbiota, thus induced in animal models (31). These studies support the reducing the likelihood of the mammalian immune system concept that diverse impairments of hematopoietic and non- mounting an overreactive response to commensal bacteria. hematopoietic cell signaling pathways underlie abnormal host- However, when the epithelial barrier is compromised by chem- microbiota interactions. ical, pathogenic, or inflammatory insults, the immune system Environmental and lifestyle risk factors also play a role in must deal with the resulting influx of commensal and opportu- disease development (23), as evidenced by modest disease nistic microorganisms. In most contexts, the immune system concordance between monozygotic twins who develop ulcer- responds appropriately to protect the host from invasive mi- ative colitis and CD in adulthood (32). For example, diet is crobes while maintaining long-term tolerance to the microbiota. implicated in causative and preventative roles in IBD through Not surprisingly, sustained breakdown of the intestinal barrier is various mechanisms (33). Of note, short- and long-term die- linked to several chronic inflammatory diseases, although the tary patterns can modify the composition of the gut microbiota mechanisms are still being determined (19, 20) (Fig. 1B). (34–36). Diet’s link to IBD, among other environmental risk In this review, we assess how functional interactions between factors that alter the gut microbiota, such as antibiotic use, has the mammalian immune system and the microbiota in the gut motivated investigation of associations between microbial can drive inflammatory diseases locally and systemically. dysbiosis and intestinal inflammation. Dysbiosis is defined as a Comparatively, we also examine settings in which host-microbiota microbial imbalance resulting in a shift (i.e., loss or outgrowth interactions can prevent or constrain autoimmune disease. Lastly, of a species) and
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