<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Annals of the Russian academy of medical sciences</journal-id><journal-title-group><journal-title xml:lang="en">Annals of the Russian academy of medical sciences</journal-title><trans-title-group xml:lang="ru"><trans-title>Вестник Российской академии медицинских наук</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0869-6047</issn><issn publication-format="electronic">2414-3545</issn><publisher><publisher-name xml:lang="en">"Paediatrician" Publishers LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1238</article-id><article-id pub-id-type="doi">10.15690/vramn1238</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>INTERNAL DISEASES: CURRENT ISSUES</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>АКТУАЛЬНЫЕ ВОПРОСЫ ВНУТРЕННИХ БОЛЕЗНЕЙ</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Modulation of instinal microbiom in the formation and progression of ulterative colitis.</article-title><trans-title-group xml:lang="ru"><trans-title>Модуляция интестинального микробиома в формировании и прогрессировании язвенного колита</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9252-9152</contrib-id><contrib-id contrib-id-type="spin">6103-6690</contrib-id><name-alternatives><name xml:lang="en"><surname>Bikbavova</surname><given-names>G. R.</given-names></name><name xml:lang="ru"><surname>Бикбавова</surname><given-names>Г. Р.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Associate Professor</p></bio><bio xml:lang="ru"><p>к.м.н., доцент</p></bio><email>galiya1976@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6581-7017</contrib-id><contrib-id contrib-id-type="spin">1961-4082</contrib-id><name-alternatives><name xml:lang="en"><surname>Livzan</surname><given-names>M. A.</given-names></name><name xml:lang="ru"><surname>Ливзан</surname><given-names>М. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Professor</p></bio><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><email>mlivzan@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Omsk State Medical University</institution></aff><aff><institution xml:lang="ru">Омский государственный медицинский университет</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2020-12-15" publication-format="electronic"><day>15</day><month>12</month><year>2020</year></pub-date><volume>75</volume><issue>6</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>577</fpage><lpage>584</lpage><history><date date-type="received" iso-8601-date="2019-11-06"><day>06</day><month>11</month><year>2019</year></date><date date-type="accepted" iso-8601-date="2020-12-08"><day>08</day><month>12</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2020, "Paediatrician" Publishers LLC</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2020, Издательство "Педиатръ"</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="en">"Paediatrician" Publishers LLC</copyright-holder><copyright-holder xml:lang="ru">Издательство "Педиатръ"</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2022-02-05"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://vestnikramn.spr-journal.ru/jour/about/submissions</ali:license_ref></license></permissions><self-uri xlink:href="https://vestnikramn.spr-journal.ru/jour/article/view/1238">https://vestnikramn.spr-journal.ru/jour/article/view/1238</self-uri><abstract xml:lang="en"><p><italic>In recent decades, an increase in the incidence of ulcerative colitis has been observed throughout the world. The purpose of this review is to generalize the available information on the influence of environmental factors and intestinal microbiome on the occurrence and development of ulcerative colitis, the role of bacteria metabolism products in the pathogenesis of the disease. Studied literature, we came to the conclusion that lifestyle in the era of post-industrial society has a significant impact on the microbial composition of the intestine and leads to changes in its diversity in patients suffering from ulcerative colitis. The changes include a decrease in the number of residential flora with anti-inflammatory activity, which synthesize short-chain fatty acids, and an increase in the number of potentially pathogenic and pathogenic microorganisms. Within the phylums Firmicutes and Proteobacteria, the proportional ratio changes. The combination of aggression factors (deterioration of the intestinal microbiome composition, the presence of aggressive intestinal metabolites) leads to intestinal mucosa permeability disfunction, impairing its barrier function. Food and bacterial agents can penetrate deeper layers of the intestinal wall through mucosal defects, which then stimulate the development of inflammatory and immune responses.</italic></p></abstract><trans-abstract xml:lang="ru"><p><italic>Целью подготовки обзора является обобщение имеющейся информации о влиянии факторов окружающей среды и микробиома кишечника на возникновение и развитие язвенного колита, роли продуктов метаболизма бактерий в патогенезе этого заболевания. Изучив литературные источники, мы пришли к выводу, что образ жизни в эпоху постиндустриального общества оказывает существенное влияние на микробный пейзаж кишечника и приводит к изменению его разнообразия у больных, страдающих язвенным колитом, в частности к уменьшению числа резидентной флоры с противовоспалительной активностью, синтезирующих короткоцепочечные жирные кислоты, и увеличению числа условно-патогенных и патогенных микроорганизмов. Внутри филумов Firmicutes и Proteobacteria изменяется пропорциональное соотношение. Совокупность факторов агрессии (нарушения состава кишечного микробиома, наличия агрессивных кишечных метаболитов) приводит к нарушению проницаемости слизистой оболочки кишки, снижается ее барьерная функция. Через дефекты слизистой оболочки в более глубокие слои стенки кишки могут проникать пищевые и бактериальные агенты, которые затем стимулируют развитие воспалительных и иммунных реакций.</italic></p></trans-abstract><kwd-group xml:lang="en"><kwd>ulcerative colitis</kwd><kwd>microbiome</kwd><kwd>environmental factors</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>язвенный колит</kwd><kwd>микробиота</kwd><kwd>факторы окружающей среды</kwd></kwd-group><funding-group><award-group><funding-source><institution-wrap><institution xml:lang="ru">Грант Президента Российской Федерации</institution></institution-wrap><institution-wrap><institution xml:lang="en">Grant of the President of the Russian Federation</institution></institution-wrap></funding-source><award-id>НШ-2558.2020.7</award-id></award-group></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Ramos GP, Papadakis KA. Mechanisms of Disease: Inflammatory Bowel Diseases. Mayo Clin. Proc. 2019;94(1):155–165. doi: https://doi.org/10.1016/j.mayocp.2018.09.013</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Ungaro R, Mehandru S, Allen PB, et al. Ulcerative colitis. Lancet. 2017;389(10080):1756–1770. doi: https://doi.org/10.1016/s0140-6736(16)32126-2</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. Gastroenterology &amp; Hepatology. 2020;5(1):17–30. doi: https://doi.org/10.1016/S2468-1253(19)30333-4</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Shouval DS, Rufo PA. The role of environmental factors in the pathogenesis of inflammatory bowel diseases: a review. JAMA Pediatr. 2017;171:999–1005. doi: https://doi.org/10.1001/jamapediatrics.2017.2571</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Kaplan GG, Ng SC. Understanding and preventing the global increase of inflammatory bowel disease. Gastroenterology. 2017;152(2):313–321. doi: https://doi.org/10.1053/j.gastro.2016.10.020</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Ng SC. Epidemiology of inflammatory bowel disease: focus on Asia. Best Pract Res Clin Gastroenterol. 2014;28(3):363–372. doi: https://doi.org/10.1016/j.bpg.2014.04.003</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Kaplan GG. The global burden of IBD: From 2015 to 2025. Nat Rev. Gastroenterol Hepatol. 2015;12(12):720–727. doi: https://doi.org/10.1038/nrgastro.2015.150</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Бикбавова Г.Р., Ливзан М.А., Совалкин В.И., и др. Влияние особенностей современного образа жизни на возникновение язвенного колита // Архив внутренней медицины. — 2019. — № 3. — С. 188–194. [Bikbavova GR, Livzan MA, Sovalkin VI, et al. Modern lifestyle and its impact on the ulcerative colitis incidence. Archiv Vnutrennei Medicini. 2019;(3):188–194. (In Russ.)]. doi: https://doi.org/10.20514/2226-6704-2019-9-3-188-193</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Kvasnovsky CL, Aujla U, Bjarnason I. Nonsteroidal anti-inflammatory drugs and exacerbations of inflammatory bowel disease. Scand J Gastroenterol. 2015;50(3):255–263. doi: https://doi.org/10.3109/00365521.2014.966753</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Cornish JA, Tan E, Simillis C, et al. The risk of oral contraceptives in the etiology of inflammatory bowel disease: a meta-analysis. Am J Gastroenterol. 2008;103(9):2394–2400. doi: https://doi.org/10.1111/j.1572-0241.2008.02064.x</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Hviid A, Svanstrom H, Frisch M. Antibiotic use and inflammatory bowel diseases in childhood. Gut. 2011;60(1):49–54. doi: https://doi.org/10.1136/gut.2010.219683</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Alhusayen RO, Juurlink DN, Mamdani MM, et al. Isotretinoinuse and the risk of inflammatory bowel disease: a population-based cohort study. J Invest Dermatol. 2013;133(4):907–912. doi: https://doi.org/10.1038/jid.2012.387</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Khalili H, Huang ES, Ananthakrishnan AN, et al. Geographical variation and incidence of inflammatory bowel disease among US women. Gut. 2012;61(12):1686–1692. doi: https://doi.org/10.1136/gutjnl-2011-301574</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Burke KE, Boumitri C, Ananthakrishnan AN. Modifiable environmental factors in inflammatory bowel disease. Cur Gastroenterol Rep. 2017;19(5):21. doi: https://doi.org/10.1007/s11894-017-0562-0</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Sasaki M, Klapproth J-MA. The Role of Bacteria in the Pathogenesis of Ulcerative Colitis. J Signal Transduct. 2012;2012:704953. doi: https://doi.org/10.1155/2012/70495</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Galley JD, Nelson MC, Yu Z, et al. Exposure to a social stressor disrupts the community structure of the colonic mucosa-associated microbiota. BMC Microbiol. 2014;14:189. doi: https://doi.org/10.1186/1471-2180-14-189</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Бикбавова Г.Р., Ливзан М.А., Совалкин В.И., и др. Психологический стресс — фактор риска развития язвенного колита? // Доказательная гастроэнтерология. — 2019. — Т. 8. — № 2. — С. 37–42. [Bikbavova GR., Livzan MA, Sovalkin VI, et al. Is psychological stress a risk factor for ulcerative colitis? Dokazatel’naya Gastroenterologia. 2019;8(2):37–42. (In Russ.)]. doi: https://doi.org/10.17116/dokgastro2019802137</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Mukhtar K, Nawaz H, Abid S. Functional gastrointestinal disorders and gut-brain axis: What does the future hold? Wolrd J. Gastroenterol. 2019;25(5):552–566. doi: https://doi.org/10.3748/wjg.v25.i5.552</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Brzozowski B, Mazur-Bialy A, Pajdo R, et al. Mechanisms by which Stress Affects the Experimental and Clinical Inflammatory Bowel Disease (IBD): Role of Brain-Gut Axis. Cur Neuropharmacol. 2016;14(8);892–900. doi: https://doi.org/10.2174/1570159x14666160404124127</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Uniken VW, Voskuil MD, Dijkstra G, et al. The genetic background of inflammatory bowel disease: from correlation to causality. J Pathol. 2017;241(2):146–58. doi: https://doi.org/10.1002/path.4817</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Childers RE, Eluri S, Vazquez C, et al. Family history of inflammatory bowel disease among patients with ulcerative colitis: a systematic review and meta-analysis. Crohns Colitis. 2014;8(11):1480–1497. doi: https://doi.org/10.1016/j.crohns.2014.05.008</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Khalif I, Shapina M. Inflammatory bowel disease treatment in Eastern Europe: current status, challenges and needs. Curr Opin Gastroenterol. 2017;33(4):230–233. doi: https://doi.org/10.1097/mog.0000000000000370</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Ursell L, Haiser HJ, Van Treuren W, et al. The intestinal metabolome: an intersection between microbiota and host. Gastroenterol. 2014;146(6):1470–1476. doi: https://doi.org/10.1053/j.gastro.2014.03.001</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Almeida A, Mitchell AL, Boland M, et al. A new genomic blueprint of the human gut microbiota. Nature. 2019;568(7753):499–504. doi: https://doi.org/10.1099/acmi.ac2019.po0041</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Kivity S, Agmon-Levin N, Blank M, et al. Infections and autoimmunity are friends or foes? Trends Immunol. 2009;30(8):409–414. doi: https://doi.org/10.1016/j.it.2009.05.005</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Strachan DP, Taylor EM, Carpenter RG. Family structure, neonatal infection, and hay fever in adolescence. Arch Dis Child. 1996;74(5):422–426. doi: https://doi.org/10.1136/adc.74.5.422</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357:266–281. doi: https://doi.org/10.1056/nejmra070553</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Sekirov I, Russell SL, Antunes LC, Finlay BB. Gut microbiota in health and disease. Physiol Rev. 2010;90(3):859–904. doi: 10.1152/physrev.00045.2009</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Jandhyala SM, Talukdar R, Subramanyam C, et al. Role of the normal gut microbiota. World J Gastroenterol. 2015;21(29):8787–8803. doi: https://doi.org/10.3748/wjg.v21.i29.8787</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>Swidsinski A, Loening-Baucke V, Lochs H, Hale LP. Spatial organization of bacterial flora in normal and inflamed intestine: a fluorescence in situ hybridization study in mice. World J Gastroenterol. 2005;11(8):1131–1140. doi: https://doi.org/10.3748/wjg.v11.i8.1131</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Aleksandrova K, Romero-Mosquera B, Hernandez V. Diet. Gut microbiome and epigenetics: Emerging links with inflammatory bowel diseases and prospects for management and prevention. Nutrients. 2017;9(9):962. doi: https://doi.org/10.3390/nu9090962</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Мазанкова Л.Н., Рыбальченко О.В., Николаева И.В. Микродисбиоз и эндогенные инфекции: руководство для врачей. — М.: ГЭОТАР-Медиа, 2018. [Mazankova LN, Pybalchenko OV, Nikolaeva IV. Microdisbioz i endogennie infekcii: rukovodstvo dlya vrachei. Moscow, GEOTAR-Media; 2018 (In Russ.)].</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Andoh A. Physiological role of gut microbiota for maintaining human health. Digestion. 2016;93(3):176–181. doi: https://doi.org/10.1159/000444066</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>Morrison DJ, Preston T. Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism. Gut Microbes. 2016;7(3):189–200. doi: https://doi.org/10.1080/19490976.2015.1134082</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Kim S, Kim JH, Park BO, Kwak YS. Perspectives on the therapeutic potential of short-chain fatty acid receptors. BMB Rep. 2014;47(3):173–178. doi: https://doi.org/10.1016/j.mayocp.2018.09.013</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Qin J, Li R, Raes J, Arumugam M, et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010;464:59–65. doi: https://doi.org/10.1038/nature0882</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Arumugam M, Raes J, Pelletier E, et al. Enterotypes of the human gut microbiome. Nature. 2011;473(7346):174–180. doi: https://doi.org/10.1038/nature09944</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Arora T, Bäckhed F. The gut microbiota and metabolic disease: current understanding and future perspectives. J Intern Med. 2016;280(4):339–349. doi: https://doi.org/10.1111/joim.12508</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Koren O, Knights D, Gonzalez A, et al. A Guide to Enterotypes across the Human Body: Meta-Analysis of Microbial Community Structures in Human Microbiome Datasets. PLoS Comput Biol. 2013;9(1):e1002863. doi: https://doi.org/10.1371/journal.pcbi.1002863</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Wu GD, Chen J, Homann C, et al. Linking long-term dietary patterns with gut microbial enterotypes. Science. 2011;334(6052):105–108. doi: https://doi.org/10.1126/science.1208344</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>De Filippo C, Cavalieri D, Di Paola M, et al. Impact of diet in shaping gut microbiotarevealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci USA. 2010;107(33):14691–14696. doi: https://doi.org/10.1073/pnas.1005963107.</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Khalili H, Chan SSM, Lochhead P, et al. The role of diet in the aetiopathogenesis of inflammatory bowel disease. Nat. Rev. Gastroenterol. Hepatol. 2018;15(9):525–535. doi: 10.1038/s41575-018-0022-9</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Gentile CL, Weir TL. The gut microbiota at the intersection of diet and human health. Science. 2018;362(6416):776–780. doi: https://doi.org/10.1126/science.aau5812</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Vangay P, Johnson AJ, Ward TL, et al. US immigration westernizes the human gut microbiome. Cell. 2018;175(4):962–972. doi: https://doi.org/10.1016/j.cell.2018.10.029</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Вялов С.С. Нарушение проницаемости слизистой оболочки как фактор патогенеза функциональных нарушений желудочно-кишечного тракта: обоснование и возможности коррекции // Consilium Medicum. — 2018. — Т. 20. — № 12. — С. 99–104. [Vialov SS. Mucosal permeability disturbances as a pathogenesis factor of gastrointestinal tract functional disorders: rationale and correction possibilities. Consilium Medicum. 2018;20(12):99–104. (In Russ.)]. doi: https://doi.org/10.26442/20751753.2018.12.180062</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Lozupone CA, Stombaugh J, Gonzalez A, et al. Meta-analyses of studies of the human microbiota. Genome Res. 2013;23(10):1704–1714. doi: https://doi.org/10.1101/gr.151803.112</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Kriss M, Hazleton KZ, Nusbacher NM, et al. Low diversity gut microbiota dysbiosis: drivers, functional implications and recovery. Curr Opin Microbiol. 2018;44:34–40. doi: https://doi.org/10.1016/j.mib.2018.07.003</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Blaser MJ, Falkow S. What are the consequences of the disappearing human microbiota? Nat Rev Microbiol. 2009;7(12):887–894. doi: https://doi.org/10.1038/nrmicro2245</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>De Souza HS, Fiocchi C. Immunopathogenesis of IBD: Current state of the art. Nat Rev Gastroenterol Hepatol. 2016;13(1):13–27. doi: https://doi.org/10.1038/nrgastro.2015.186</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Hall AB, Yassour M, Sauk J, et al. A novel Ruminococcus gnavus clade enriched in inflammatory bowel disease patients. Genome Med. 2017;9(1):103. doi: https://doi.org/10.1186/s13073-017-0490-5</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Henke MT, Kenny DJ, Cassilly CD, et al. Ruminococcus gnavus, a member of the human gut microbiome associated with Crohn’s disease, produces an inflammatory polysaccharide. Proc Natl Acad Sci USA. 2019;116(26):12672–12677. doi: https://doi.org/10.1073/pnas.1904099116</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Yang G. Hydrogen sulfide in cell survival: A double-edged sword. Expert Rev Clin Pharmacol. 2011;4(1):33–47. doi: https://doi.org/10.1586/ecp.10.131</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Barton LL, Ritz NL, Fauque GD, Lin H.C. Sulfur Cycling and the Intestinal Microbiome. Dig Dis Sci. 2017;62(9):2241–2257. doi: https://doi.org/10.1007/s10620-017-4689-5</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Anantharaman K, Hausmann B, Jungbluth SP, et al. Expanded diversity of microbial groups that shape the dissimilatory sulfur cycle. ISME J. 2018;12(7):1715–1728. doi: https://doi.org/10.1038/s41396-018-0078-0</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>Nagao-Kitamoto H, Kitamoto S, Kuffa P, Kamada N. Pathogenic role of the gut microbiota in gastrointestinal diseases. Intest Res. 2016;14(2):127–138. doi: https://doi.org/10.5217/ir.2016.14.2.127</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Iszatt N, Janssen S, Lenters V, et al. Environmental toxicants in breast milk of Norwegian mothers and gut bacteria composition and metabolites in their infants at 1 month. Microbiome. 2019;7(1):34. doi: https://doi.org/10.1186/s40168-019-0645-2</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>Morgan XC, Tickle TL, Sokol H, et al. Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment. Genome Biol. 2012;13(9):R79. doi: https://doi.org/10.1186/gb-2012-13- 9-r79</mixed-citation></ref><ref id="B58"><label>58.</label><mixed-citation>Zeng MY, Inohara N, Nuñez G. Mechanisms of inflammation-driven bacterial dysbiosis in the gut. Mucosal Immunol. 2017;10(1):18–26. doi: https://doi.org/10.1038/mi.2016.75</mixed-citation></ref><ref id="B59"><label>59.</label><mixed-citation>Food Availability (Per Capita) Data System (Table: Sugar and sweeteners) [updated 2019 Aug 26; cited 2019 May 6]. Available from: https://www.ers.usda.gov/data-products/food-availability-per-capita-data-system</mixed-citation></ref><ref id="B60"><label>60.</label><mixed-citation>Laffin M, Fedorak R, Zalasky A, et al. A high-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice. Sci Rep. 2019;9(1):12294. doi: 10.1038/s41598-019-48749-2</mixed-citation></ref><ref id="B61"><label>61.</label><mixed-citation>Martinez-Medina M, Garcia-Gil LJ. Escherichia coli in chronic inflammatory bowel diseases: An update on adherent invasive Escherichia coli pathogenicity. World J Gastrointest Pathophysiol. 2014;5(3):213–227. doi: https://doi.org/10.4291/wjgp.v5.i3.213</mixed-citation></ref><ref id="B62"><label>62.</label><mixed-citation>Gonze D, Coyte KZ, Lahti L, Faust K. Microbial communities as dynamical systems. Curr Opin Microbiol. 2018;44:41–49. doi: https://doi.org/10.1016/j.mib.2018.07.004</mixed-citation></ref><ref id="B63"><label>63.</label><mixed-citation>Макейкина М.А., Ливзан М.А. Генетические прогностические факторы течения неспецифического язвенного колита // Практическая медицина. — 2012. — Т. 9. — № 65. — С. 133–136. [Makeikina MA, Livzan MA. Genetic prognostic factors of course of nonspecific ulcerative colitis. Prakticheskaya medicina. 2012;9(65):133–136. (In Russ.)]</mixed-citation></ref><ref id="B64"><label>64.</label><mixed-citation>Neurath MF. Cytokines in inflammatory bowel disease. Nat Rev Immunol. 2014;14(5):329–342. doi: https://doi.org/10.1038/nri3661</mixed-citation></ref></ref-list></back></article>
