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Научно-практическая ревматология

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Концепция «болезни барьерного органа» в патогенезе спондилоартритов

https://doi.org/10.14412/1995-4484-2016-199-205

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Аннотация

В настоящее время созданы предпосылки для изменения научного взгляда на этиологию и патогенез спондилоартритов (СпА). Важная роль отводится нарушению функционирования и целостности так называемых барьерных органов, выстраивающих защиту человека между его внутренней и внешней средой. Современные данные о клеточно-молекулярных механизмах патогенеза СпА позволяют ревматологам выдвинуть гипотезу о концепции «болезни барьерного органа» как доклинической стадии развития заболеваний, входящих в группу СпА. Существуют основания предполагать, что в этом процессе задействованы индивидуальные генетические и иммунные факторы, приводящие к повреждению поверхностного эпителия слизистых оболочек и эпидермиса, который служит первым защитным барьером врожденного иммунитета и находится в контакте с чрезвычайно большим количеством микроорганизмов (микробиомом) и с патоген-ассоциированными молекулярными структурами. Микробиом может оказывать влияние на доклиническую фазу болезни несколькими способами, в том числе путем изменений состава микрофлоры (дисбиоз), а также действуя в качестве мишеней иммунологической дисрегуляции. 

Об авторах

Е. А. Галушко
ФГБНУ Научно- исследовательский институт ревматологии им. В.А. Насоновой, Москва
Россия

учебно-методический отдел с центром информационных технологий

заведующая отделом, докт. мед. наук



А. В. Гордеев
ФГБНУ Научно- исследовательский институт ревматологии им. В.А. Насоновой, Москва
Россия

лаборатория микроциркуляции и воспаления

ведущий научный сотрудник лаборатории, докт. мед. наук



Список литературы

1. Насонов ЕЛ, Александрова ЕН, Новиков АА. Аутоиммунные ревматические заболевания: итоги и перспективы научных исследований. Научно-практическая ревматология. 2015;53(3):230-7. [Nasonov EL, Aleksandrova EN, Novikov AA. Autoimmune rheumatic diseases: Results and prospects for researches. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2013;53(3):230-7 (In Russ.)]. doi: 10.14412/1995-4484-2015-230-237

2. Новиков АА, Александрова ЕН, Насонов ЕЛ. Протеомные исследования в ревматологии. Научно-практическая ревматология. 2012;50(6):56-62 [Novikov AA, Aleksandrova EN, Nasonov EL. Proteomic studies in rheumatology. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2012;50(6):56-62. (In Russ.)]. doi: 10.14412/1995-4484-2012-1295

3. Raza K, Gerlag DM. Preclinical inflammatory rheumatic diseases. Rheum Dis Clin North Am. 2014 Nov;40(4):569-80. doi: 10.1016/j.rdc.2014.07.001

4. Buckley CD, Gilroy DW, Serhan CN, et al. The resolution of inflammation. Nat Rev Immunol. 2013;13(1):59-66. doi: 10.1038/nri3362

5. Goldblatt F, O'Neill SG. Clinical aspects of autoimmune rheumatic diseases. Lancet. 2013;382:797-808. doi: 10.1016/S0140- 6736(13)61499-3

6. Cho JH, Gregersen PK. Genomics and the multifactorial nature of human autoimmune disease. New Engl J Med. 2011;365:1612- 23. doi: 10.1056/NEJMra1100030

7. Kuhn KA, Pedraza I, Demoruelle K. Mucosal immune responses to microbiota in the development of autoimmune disease. Rheum Dis Clin N Am. 2014;40:711-25. doi: 10.1016/j.rdc.2014.07.013

8. Kriegel MA. Self or non-self? The multifaceted role of the microbiota in immune-mediated diseases. Clin Immunol. 2015 Aug;159(2):119-21. doi: 10.1016/j.clim.2015.05.010

9. Costello ME, Robinson PC, Benham H, Brown MA. The intestinal microbiome in human disease and how it relates to arthritis and spondyloarthritis. Best Pract Res Clin Rheumatol. 2015 Apr;29(2):202-12. doi: 10.1016/j.berh.2015.08.001

10. Backhed F, Ley RE, Sonnenburg JL, et al. Host-bacterial mutual￾ism in the human intestine. Science. 2005;307:1915-20. doi: 10.1126/science.1104816

11. Consortium HMP. Structure, function and diversity of the healthy human microbiome. Nature. 2012;486:207-14. doi: 10.1038/nature11234

12. Qin J, Li R, Raes J, et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010;464:59-65. doi: 10.1038/nature08821

13. Clarridge III JE. Impact of 16S rRNA gene sequence analysis for identification of bacteria on clinical microbiology and infectious diseases. Clin Microbiol Rev. 2004;17(4):840-62. doi: 10.1128/CMR.17.4.840-862.2004

14. Huse SM, Dethlefsen L, Huber JA, et al. Exploring microbial diversity and taxonomy using SSU rRNA hypervariable tag sequencing. PLoS Genet. 2008;4(11):e1000255. doi: 10.1371/journal.pgen.1000255

15. Morgan XC, Segata N, Huttenhower C. Biodiversity and functional genomics in the human microbiome. Trends Genet. 2013;29:51-8. doi: 10.1016/j.tig.2012.09.005

16. Group TNHW, Peterson J, Garges S, et al. The NIH human microbiome project. Genome Res. 2009;19(12):2317-23. doi: 10.1101/gr.096651.109

17. Caporaso JG, Lauber C, Costello E, et al. Moving pictures of the human microbiome. Genome Biol. 2011;12(5):R50. doi: 10.1186/gb-2011-12-5-r50

18. Arumugam M, Raes J, Pelletier E, et al. Enterotypes of the human gut microbiome. Nature. 2011;473:174-80. doi: 10.1038/nature09944

19. 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: 10.1371/journal.pcbi.1002863

20. Gomez A, Luckey D, Taneja V. The gut microbiome in autoimmunity: Sex matters. Clin Immunol. 2015 Aug;159(2):154-62. doi: 10.1016/j.clim.2015.04.016. Epub 2015 May 6. 21. Knights D, Ward TL, McKinlay CE, et al. Rethinking «enterotypes». Cell Host Microbe. 2014;16(4):433-7. doi: 10.1016/j.chom.2014.09.013

21. Ruff WE, Kriegel MA. Autoimmune host-microbiota interactions at barrier sites and beyond. Trends Mol Med. 2015 Apr;21(4):233- 44. doi: 10.1016/j.molmed.2015.02.006

22. Stoll ML. Gut microbes, immunity, and spondyloarthritis. Clin Immunol. 2015;159(2):134-42. doi: 10.1016/j.clim.2015.05.001

23. Huttenhower C, Kostic AD, Xavier RJ. Inflammatory bowel disease as a model for translating the microbiome. Immunity. 2014;40:843-54. doi: 10.1016/j.immuni.2014.05.013

24. Costello ME, Ciccia F, Willner D, et al. Intestinal dysbiosis in ankylosing spondylitis. Arthritis Rheum. 2014 Nov 21. doi: 10.1002/art.38967. [Epub ahead of print].

25. Gao Z, Tseng CH, Strober BE, et al. Substantial alterations of the cutaneous bacterial biota in psoriatic lesions. PLoS One. 2008; Jul 23;3(7):e2719. doi: 10.1371/journal.pone.0002719

26. Эрдес ШФ. Является ли псориатический артрит действительно псориатическим? Научно-практическая ревматология. 2014;52(6):678-81 [Erdes SF. Is psoriatic arthritis really psoriatic? Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2014;52(6):678-81 (In Russ.)]. doi: 10.14412/1995-4484-2014-678-681

27. Lekpa FK, Wendling D, Claudepierre P. Spondyloarthritis: criteria, limitations, and perspectives throughout history. Joint Bone Spine. 2014;18(6):759-65. doi: 10.1016/j.jbspin.2015.02.017

28. Wendling D, Claudepierreb P, Pratia C, Dougadosc M. Spondyloarthritis: A concept or a disease? Joint Bone Spine. 2015;82(6):387-9. doi: 10.1016/j.jbspin.2015.06.006

29. Насонов ЕЛ, Галушко ЕА, Гордеев АВ. Современный взгляд на патогенез спондилоартритов – молекулярные механизмы. Научно-практическая ревматология. 2015;53(3):299-307 [Galushko EA, Gordeev AV. Modern idea on the pathogenesis of spondyloarthritis: Molecular mechanisms. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2013;53(3):299- 307 (In Russ.)]. doi: 10.14412/1995-4484-2015-299-307

30. Jacques P, van Praet L, Carron P, et al. Pathophysiology and role of the gastrointestinal system in spondyloarthritides. Rheum Dis Clin North Am. 2012 Aug;38(3):569-82. doi: 10.1016/j.rdc.2012.08.012

31. Schaeverbeke T, Truchetet ME, Richez C. Gut metagenome and spondyloarthritis. Joint Bone Spine. 2013 Jul;80(4):349-52. doi: 10.1016/j.jbspin.2013.02.005

32. Van Praet L, van den Bosch FE, Jacques P, et al. Microscopic gut inflammation in axial spondyloarthritis: a multiparametric predic￾tive model. Ann Rheum Dis. 2013;72(3):414-7. doi: 10.1136/annrheumdis-2012-202135

33. Costello M-E, Ciccia F, Willner D, et al. Brief report: intestinal dysbiosis in ankylosing spondylitis. Arthritis Rheum. 2015;67(3):686-91. doi: 10.1002/art.38967

34. Scher JU, Ubeda C, Artacho A, et al. Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheum. 2015;67(1):128-39. doi: 10.1002/art.38892

35. Jostins L, Ripke S, Weersma RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119-24. doi: 10.1038/nature11582

36. Quinton JF. Anti-saccharomyces cerevisiae mannan antibodies combined with antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease: prevalence and diagnostic role. Gut. 1998;42:788-91. doi: 10.1136/gut.42.6.788

37. Targan SR. Antibodies to CBir1 flagellin define a unique response that is associated independently with complicated Crohn's disease. Gastroenterology. 2005;128:2020-8. doi: 10.1053/j.gastro.2005.03.046

38. Rashid T, Ebringer A. Ankylosing spondylitis is linked to Klebsiella the evidence. Clin Rheumatol. 2007;26(6):858-64. doi: 10.1007/s10067-006-0488-7

39. Telfer NR, Chalmers RJ, Whale K, Colman G. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128:39-42. doi: 10.1001/archderm.1992.01680110049004

40. Castelino M, Eyre S, Upton M, et al. The bacterial skin microbiome in psoriatic arthritis, an unexplored link in pathogenesis: challenges and opportunities offered by recent technological advances. Rheumatology (Oxford). 2014;53:777-84. doi: 10.1093/rheumatology/ket319

41. Belkaid Y, Hand TW. Role of the microbiota in immunity and inflammation. Cell. 2014;157:121-41. doi: 10.1016/j.cell.2014.03.011

42. Abreu MT, Fukata M, Breglio K. Innate immunity and its implications on pathogenesis of inflammatory bowel disease. In: Targan SR, Shanahan F, Karp LC, eds. Inflammatory bowel dis￾ease. Oxford: Blackwell Publishing Ltd.;2010. P.64-81.

43. Lande R, Gregorio J, Facchinetti V, et al. Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature. 2007;449:564-9. doi: 10.1038/nature06116

44. Sato S, St-Pierre C, Bhaumik P, Nieminen J. Galectins in innate immunity: dual functions of host soluble β-galactosidase-binding lectins as damage-associated molecular patterns (DAMPs) and as receptors for pathogen-associated molecular patterns (PAMPs). Immunol Rev. 2009;230:172. doi: 10.1111/j.1600-065X.2009.00790.x

45. Pancer Z, Cooper MD. The evolution of adaptive immunity. Annu Rev Immunol. 2006;24:497. doi: 10.1146/annurev.immunol.24.021605.090542

46. Fukata M, Vamadevan AS, Abreu MT. Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in inflammatory disorders. Semin Immunol. 2009;21:242. doi: 10.1016/j.smim.2009.06.005

47. Kawai T, Akira S. Pathogen recognition with Toll-like receptors. Curr Opin Immunol. 2005;17:338. doi: 10.1016/j.coi.2005.02.007

48. Ting JP, Kastner DL, Hoffman HM. CATERPILLERs, pyrin and hereditary immunological disorders. Nat Rev Immunol. 2006;6:183. doi: 10.1038/nri1788

49. Jha S, Ting JP-Y. Inflammasome-associated nucleotide-binding domain, leucinerich repeat proteins and inflammatory diseases. J Immunol. 2009;183:7623. doi: 10.4049/jimmunol.0902425

50. Blander JM, Medzhitov R. Toll-dependent selection of microbial antigens for presentation by dendritic cells. Nature. 2006;440:808 doi: 10.1038/nature04596

51. Broat H, Peppelenbosch MP, Hommes DW. Immunology of Crohn's disease. Ann NY Acad Sci. 2006;1072:135-54. doi: 10.1196/annals.1326.039

52. Mattozzi C, Richetta AG, Cantisani C, et al. Psoriasis: new insight about pathogenesis, role of barrier organ integrity, NLR/CATERPILLER family genes and microbial flora. J Dermatol. 2012 Sep;39(9):752-60. doi: 10.1111/j.1346-8138.2012.01606

53. Bos JD. Psoriasis, innate immunity, and gene pools. J Am Acad Dermatol. 2007;56(3):468-71. doi: 10.1016/j.jaad.2006.12.006

54. Biswas A, Petnicki-Ocwieja T, Kobayashi KS. Nod2: a key regulator linking microbiota to intestinal mucosal immunity. J Mol Med (Berl.). 2012;90:15-24. doi: 10.1007/s00109-011-0802-y. Epub 2011 Aug 23.

55. Strober W, Asano N, Fuss I, et al. Cellular and molecular mechanisms underlying NOD2 risk-associated polymorphisms in Crohn's disease. Immunol Rev. 2014;260:249-60. doi: 10.1111/imr.12193

56. Laukens D, Peeters H, Marichal D, et al. CARD15 gene polymorphisms in patients with spondyloarthropathies identify a specific phenotype previously related to Crohn's disease. Ann Rheum Dis. 2005;64:930-5. doi: 10.1136/ard.2004.028837

57. Faustini F, Zoli A, Ferraccioli GF. Immunologic and genetic links between spondylarthropathies and inflammatory bowel diseases. Eur Rev Med Pharmacol Sci. 2009 Mar;13 Suppl 1:1-9.

58. Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment. Clin Dev Immunol. 2013;2013:631408. doi: 10.1155/2013/631408

59. Benjamin JL, Sumpter R Jr, Levine B, et al. Intestinal epithelial autophagy is essential for host defense against invasive bacteria. Cell Host Microbe. 2013;13(6):723-34. doi: 10.1016/j.chom.2013.05.004

60. Ciccia F, Accardo-Palumbo A, Rizzo A, et al. Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis and subclinical gut inflammation. Ann Rheum Dis. 2013;73(8):1566-74. doi: 10.1136/annrheumdis-2012-202925

61. Ciccia F, Bombardieri, Rizzo A, et al. Over-expression of paneth cell-derived anti-microbial peptides in the gut of patients with ankylosing spondylitis and subclinical intestinal inflammation. Rheumatology. 2010;49:2076-83. doi: 10.1093/rheumatology/keq239

62. Lee YK, Mazmanian SK. Has the microbiota played a critical role in the evolution of the adaptive immune system? Science. 2010;330:1768-73. doi: 10.1126/science.1195568

63. Ciccia F, Accardo-Palumbo A, Giardina A, et al. Expansion of intestinal CD4+CD25(high) Treg cells in patients with ankylosing spondylitis: a putative role for interleukin-10 in preventing intes￾tinal Th17 response. Arthritis Rheum. 2010;62:3625-34. doi: 10.1002/art.27699

64. Shih VF, Cox J. Homeostatic IL-23 receptor signaling limits Th17 response through IL-22-mediated containment of commensal microbiota. Proc Natl Acad Sci USA. 2014 Sep 23;111(38):13942-7. doi: 10.1073/pnas.1323852111

65. Miossec P, Korn T, Kuchroo VK. Interleukin17 and type 17 helper T cells. N Engl J Med. 2009;361:888-98. doi: 10.1056/NEJMra0707449

66. Эрдес ШФ, Волнухин ЕВ, Галушко ЕА. Лечение больных анкилозирующим спондилитом в реальной практике врача- ревматолога в России. Научно-практическая ревматология. 2013;51(1):15-20 [Erdes SF, Volnuhin EV, Galushko EA. Treatment in patients with ankylosing spondylitis in the real clinical practice of a rheumatologist in Russia. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2013;51(1):15- 20 (In Russ.)]. doi: 10.14412/1995-4484-2013-1195

67. Borish LC, Steinke JW. Cytokines and chemokines. J Allergy Clin Immunol. 2003;111:460-75. doi: 10.1067/mai.2003.108

68. Sedger LM, McDermott MF. TNF and TNF-receptors: From mediators of cell death and inflammation to therapeutic giants – past, present and future. Cytokine Growth Factor Rev. 2014 Aug;25(4):453-72. doi: 10.1016/j.cytogfr.2014.07.016

69. Bazzoni F, Beutler B. Tumor necrosis factor ligand and receptor families. N Engl J Med. 1996;334(26):1717-25. doi: 10.1056/NEJM199606273342607

70. Tartaglia LA, Weber RF, Figari IS, et al. The two different receptors for tumor necrosis factor mediate distinct cellular responses. Proc Natl Acad Sci USA. 1991;88:9292-6. doi: 10.1073/pnas.88.20.9292

71. Carpentier I, Coornaert B, Beyaert R. Function and regulation of tumor necrosis factor type 2. Curr Med Chem. 2004;11:2205-12. doi: 10.2174/0929867043364694

72. Gupta S, Gollapudi S. Molecular mechanisms of TNF-alphainduced apoptosis in aging human T cell subsets. Int J Biochem Cell Biol. 2005;37(5):1034-42. doi: 10.1016/j.biocel.2004.08.013

73. Grell M, Douni E, Wajant H, et al. The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptor. Cell. 1995;83:793-802. doi: 10.1016/0092-8674(95)90192-2

74. Van Hauwermeiren F, Vandenbroucke RE, Grine L, et al. TNFR1-induced lethal inflammation is mediated by goblet and Paneth cell dysfunction Mucosal Immunol. 2015 Jul;8(4):828-40. doi: 10.1038/mi.2014.112

75. Chan FK, Chun HJ, Zheng L, et al. A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling. Science. 2000;288:2351-4. doi: 10.1126/science.288.5475.2351

76. Le CT, Laidlaw G, Morehouse CA, et al. Synergistic actions of blocking angiopoietin-2 and tumor necrosis factor-α in suppressing remodeling of blood vessels and lymphatics in airway inflammation. Am J Pathol. 2015 Nov;185(11):2949-68. doi: 10.1016/j.ajpath.2015.07.010

77. Schreiber S, Rosenstiel P, Albrecht M, et al. Genetics of Crohn disease, an archetypal inflammatory barrier disease. Nat Rev Genet. 2005;6:376-88. doi: 10.1038/nrg1607. PMID:15861209

78. Skroza N, Proietti I, Pampena R, et al. Correlations between psoriasis and inflammatory bowel diseases. Biomed Res Int. 2013;2013:983902. doi: 10.1155/2013/983902. Epub 2013 Jul 21.

79. D'Agostino MA, Aegerter P, Dougados M, et al. Three phenotype profiles arerevealed by cluster analysis in early inflammatory back pain suggestive of spondyloarthritis (spa). Results from the devenir des spondyloarthropathies indifferenciees recentes (DESIR) cohort. Ann Rheum Dis 2012;71:411. doi: 10.1136/annrheumdis- 2012-eular.2746

80. Baeten D, Breban M, Lories R, et al. Are spondylarthritides related but distinct conditions or a single disease with a heterogeneous phenotype? Arthritis Rheum. 2013;65:12-20. doi: 10.1002/art.37829

81. Richette P, Tubach F, Breban M, et al. Psoriasis and phenotype of patients withearly inflammatory back pain. Ann Rheum Dis. 2013;72:566-71. doi: 10.1136/annrheumdis-2012-201610

82. Machado P, Landewe R, Braun J, et al. Ankylosing spondylitis patients with and without psoriasis do not differ in disease phenotype. Ann Rheum Dis. 2013;72:1104-7. doi: 10.1136/annrheumdis- 2012-202922


Для цитирования:


Галушко Е.А., Гордеев А.В. Концепция «болезни барьерного органа» в патогенезе спондилоартритов. Научно-практическая ревматология. 2016;54(2):199-205. https://doi.org/10.14412/1995-4484-2016-199-205

For citation:


Galushko E.A., Gordeev A.V. THE CONCEPT OF BARRIER ORGAN DISEASE IN THE PATHOGENESIS OF SPONDYLOARTHRITIS. Rheumatology Science and Practice. 2016;54(2):199-205. (In Russ.) https://doi.org/10.14412/1995-4484-2016-199-205

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ISSN 1995-4484 (Print)
ISSN 1995-4492 (Online)