Рецепт. 2020; : 893-904
Как микробиота формирует ревматические заболевания? Часть 1
https://doi.org/10.34883/PI.2020.23.6.0010Аннотация
В кишечнике человека обитает чрезвычайно разнообразное и обильное микробное сообщество, которое корректирует и даже модулирует многие процессы, связанные со здоровьем. «Интерфейсы» слизистой оболочки являются особенно активными участками взаимодействия микроорганизмов и хозяев. Возрастающее понимание характерного состава и функции микробиоты кишечника выявило, что она участвует не только в поддержании целостности слизистой оболочки, но затрагивает и гомеостаз системы иммунитета с формированием как локальных, так и системных иммунных реакций. В представленном обзоре рассмотрена роль нарушений устойчивого состояния и взаимодействия «хозяин – микроорганизм», которые могут потенциально влиять на развитие и прогрессирование ревматических заболеваний. В заключение будут рассмотрены вопросы новых терапевтических целей коррекции микробиоты.
Список литературы
1. Hand T.W., Belkaid Y. (2012) Acute gastrointestinal infection induces long-lived microbiota-specific T cell responses. Science, 337(6101), 1553–1556.
2. Ruff W.E., Kriegel M.A. (2015) Autoimmune host-microbiota interactions at barrier sites and beyond. Trends in molecular medicine, 21(4), 233–244.
3. Van Praet J.T., Donovan E., Vanassche I. (2015). Commensal microbiota influence systemic autoimmune responses. The EMBO journal, 34(4), 466–474.
4. Hooper L.V., Littman D.R., Macpherson A.J. (2012) Interactions between the microbiota and the immune system. Science, 336, 1268–1273 (2012).
5. Faria A.M., Weiner H.L. (2005) Oral tolerance. Immunol. Rev., 206, 232–259.
6. Siezen R.J., Kleerebezem, M. (2011). The human gut microbiome: are we our enterotypes? Microbial biotechnology, 4(5), 550.
7. Obata T., Goto Y., Kunisawa J. (2010). Indigenous opportunistic bacteria inhabit mammalian gut-associated lymphoid tissues and share a mucosal antibody- mediated symbiosis. Proceedings of the National Academy of Sciences, 107(16), 7419–7424.
8. Sun C.M., Hall J.A. (2007). Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid. The Journal of experimental medicine, 204(8), 1775–1785.
9. Bach J.F. (2018) The hygiene hypothesis in autoimmunity: the role of pathogens and commensals. Nat. Rev. Immunol., 18, 105–120.
10. Dowds C.M., Blumberg R.S., Zeissig S. (2015) Control of intestinal homeostasis through crosstalk between natural killer T cells and the intestinal microbiota.Clin Immunol., 159:128–133.
11. An D., Oh S.F., Olszak T., Neves (2014) Sphingolipids from a symbiotic microbe regulate homeostasis of host intestinal natural killer T cells. Cell, 156 (1–2), 123–133.
12. Knight Stella C. (1983) Induction of immune responses in vivo with small numbers of veiled (dendritic) cells. Proceedings of the National Academy of Sciences,80.19: 6032–6035.
13. Worbs T., Bode U., Yan S., Hoffmann M.W., Hintzen G., Bernhardt G. (2006) Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells. J Exp Med., 203(3):519–527.
14. Matteoli G., Mazzini E., Iliev I.D., Mileti E., Fallarino F., Puccetti P. (2010) Gut CD103+ dendritic cells express indole amine 2,3-dioxygenase which influences T regulatory/T effector cell balance and oral tolerance induction. Gut, 59(5):595–604.
15. Wang X., Sherman A., Liao G., Leong K.W., Daniell H., Terhorst C., Herzog R.W. (2013) Mechanism of oral tolerance induction to therapeutic proteins. Advanced drug delivery reviews, 65(6), 759–773.
16. Honda K, Littman D.R. (2012) The microbiome in infectious disease and inflammation. Annu Rev Immunol., 30:759–795.
17. Chang P.V., Hao L., Offermanns S., Medzhitov R. (2014) The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition. Proceedings of the National Academy of Sciences, 111(6), 2247–2252.
18. Montoya J. (2016) Patients with ankylosing spondylitis have been breast fed less often than healthy controls: a case-control retrospective study. Ann. Rheum. Dis., 75, 879–882.
19. Perez Pablo F. (2007) Bacterial imprinting of the neonatal immune system: lessons from maternal cells? Pediatrics, 119.3: e724-e732.
20. Iwata M. (2009) Retinoic acid production by intestinal dendritic cells and its role in T-cell trafficking. Semin Immunol., 21(1):8–13.
21. Kabeerdoss J., Sandhya P., Danda D. (2016) Gut inflammation and microbiome in spondyloarthritis. Rheumatology international, 36(4), 457–468.
22. Chen H., Nwe P.K., Yang Y. (2019).A forward chemical genetic screen reveals gut microbiota metabolites that modulate host physiology. Cell, 177(5), 1217–1231.
23. Rakoff-Nahoum S., Paglino J., Eslami-Varzaneh F., Edberg S., Medzhitov R. (2004) Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis. Cell, 118(2), 229–241.
24. Abaturov O., Volosovec O., Yulіsh E. (2014) Lekarstvennye sredstva, moduliruyushchie aktivnost’TLR [Drugs that modulate the activity of TLR].
25. Toussirot É., Laheurte, C., Gaugler B., Gabriel D., Saas P. (2018) Increased IL-22-and IL-17A-producing mucosal-associated invariant T cells in the peripheral blood of patients with ankylosing spondylitis. Frontiers in immunology, 9, 1610.
26. Ciccia F. (2015) Type 3 innate lymphoid cells producing IL-17 and IL-22 are expanded in the gut, in the peripheral blood, synovial fluid and bone marrow of patients with ankylosing spondylitis. Annals of the rheumatic diseases, 74(9), 1739–1747.
Recipe. 2020; : 893-904
How Does Microbiota Form Rheumatic Diseases? Part 1
https://doi.org/10.34883/PI.2020.23.6.0010Abstract
References
1. Hand T.W., Belkaid Y. (2012) Acute gastrointestinal infection induces long-lived microbiota-specific T cell responses. Science, 337(6101), 1553–1556.
2. Ruff W.E., Kriegel M.A. (2015) Autoimmune host-microbiota interactions at barrier sites and beyond. Trends in molecular medicine, 21(4), 233–244.
3. Van Praet J.T., Donovan E., Vanassche I. (2015). Commensal microbiota influence systemic autoimmune responses. The EMBO journal, 34(4), 466–474.
4. Hooper L.V., Littman D.R., Macpherson A.J. (2012) Interactions between the microbiota and the immune system. Science, 336, 1268–1273 (2012).
5. Faria A.M., Weiner H.L. (2005) Oral tolerance. Immunol. Rev., 206, 232–259.
6. Siezen R.J., Kleerebezem, M. (2011). The human gut microbiome: are we our enterotypes? Microbial biotechnology, 4(5), 550.
7. Obata T., Goto Y., Kunisawa J. (2010). Indigenous opportunistic bacteria inhabit mammalian gut-associated lymphoid tissues and share a mucosal antibody- mediated symbiosis. Proceedings of the National Academy of Sciences, 107(16), 7419–7424.
8. Sun C.M., Hall J.A. (2007). Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid. The Journal of experimental medicine, 204(8), 1775–1785.
9. Bach J.F. (2018) The hygiene hypothesis in autoimmunity: the role of pathogens and commensals. Nat. Rev. Immunol., 18, 105–120.
10. Dowds C.M., Blumberg R.S., Zeissig S. (2015) Control of intestinal homeostasis through crosstalk between natural killer T cells and the intestinal microbiota.Clin Immunol., 159:128–133.
11. An D., Oh S.F., Olszak T., Neves (2014) Sphingolipids from a symbiotic microbe regulate homeostasis of host intestinal natural killer T cells. Cell, 156 (1–2), 123–133.
12. Knight Stella C. (1983) Induction of immune responses in vivo with small numbers of veiled (dendritic) cells. Proceedings of the National Academy of Sciences,80.19: 6032–6035.
13. Worbs T., Bode U., Yan S., Hoffmann M.W., Hintzen G., Bernhardt G. (2006) Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells. J Exp Med., 203(3):519–527.
14. Matteoli G., Mazzini E., Iliev I.D., Mileti E., Fallarino F., Puccetti P. (2010) Gut CD103+ dendritic cells express indole amine 2,3-dioxygenase which influences T regulatory/T effector cell balance and oral tolerance induction. Gut, 59(5):595–604.
15. Wang X., Sherman A., Liao G., Leong K.W., Daniell H., Terhorst C., Herzog R.W. (2013) Mechanism of oral tolerance induction to therapeutic proteins. Advanced drug delivery reviews, 65(6), 759–773.
16. Honda K, Littman D.R. (2012) The microbiome in infectious disease and inflammation. Annu Rev Immunol., 30:759–795.
17. Chang P.V., Hao L., Offermanns S., Medzhitov R. (2014) The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition. Proceedings of the National Academy of Sciences, 111(6), 2247–2252.
18. Montoya J. (2016) Patients with ankylosing spondylitis have been breast fed less often than healthy controls: a case-control retrospective study. Ann. Rheum. Dis., 75, 879–882.
19. Perez Pablo F. (2007) Bacterial imprinting of the neonatal immune system: lessons from maternal cells? Pediatrics, 119.3: e724-e732.
20. Iwata M. (2009) Retinoic acid production by intestinal dendritic cells and its role in T-cell trafficking. Semin Immunol., 21(1):8–13.
21. Kabeerdoss J., Sandhya P., Danda D. (2016) Gut inflammation and microbiome in spondyloarthritis. Rheumatology international, 36(4), 457–468.
22. Chen H., Nwe P.K., Yang Y. (2019).A forward chemical genetic screen reveals gut microbiota metabolites that modulate host physiology. Cell, 177(5), 1217–1231.
23. Rakoff-Nahoum S., Paglino J., Eslami-Varzaneh F., Edberg S., Medzhitov R. (2004) Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis. Cell, 118(2), 229–241.
24. Abaturov O., Volosovec O., Yulіsh E. (2014) Lekarstvennye sredstva, moduliruyushchie aktivnost’TLR [Drugs that modulate the activity of TLR].
25. Toussirot É., Laheurte, C., Gaugler B., Gabriel D., Saas P. (2018) Increased IL-22-and IL-17A-producing mucosal-associated invariant T cells in the peripheral blood of patients with ankylosing spondylitis. Frontiers in immunology, 9, 1610.
26. Ciccia F. (2015) Type 3 innate lymphoid cells producing IL-17 and IL-22 are expanded in the gut, in the peripheral blood, synovial fluid and bone marrow of patients with ankylosing spondylitis. Annals of the rheumatic diseases, 74(9), 1739–1747.
