EN PL
REVIEW PAPER
New aspects of spondyloarthritis pathogenesis. Part II – environmental factors, microbiome disturbances, extra-articular symptoms
 
 
More details
Hide details
 
Submission date: 2014-04-03
 
 
Acceptance date: 2014-05-26
 
 
Online publication date: 2014-07-31
 
 
Publication date: 2014-06-30
 
 
Reumatologia 2014;52(3):172-180
 
KEYWORDS
TOPICS
ABSTRACT
Spondyloarthritis (SpA) is a group of inflammatory diseases with overlapping clinical features, which also share a genetic background. Bacterial infections of the gastrointestinal or genitourinary tract are the most important environmental factors associated with SpA development. Recent data show that intracellular bacteria may spread the infection to other anatomical locations. In patients suffering from SpA, extra-articular manifestations, especially intestinal inflammation, are common. Recent progress in understanding the role of intestinal microbiota in gut homeostasis and accumulating data showing the implication of microbiome disruption in the development of various diseases also shed more light on SpA pathogenesis. It is proposed that SpA may originate from the relocation to the joints of the immune response induced primarily in the gut. The intestinal dysbiosis caused by genetic and environmental factors is the most likely cause of SpA-associated gut inflammation.
 
REFERENCES (50)
1.
Kontny E. Nowe aspekty patogenezy spondyloartropatii za­palnych. Część I – uwarunkowania genetyczne, rola cząsteczek HLA-B27. Reumatologia 2014; 52: 105-111. .
 
2.
Chorus AM, Miedema HS, Boonen A, et al. Quality of life and work in patients with rheumatoid arthritis and ankylosing spondylitis of working age. Ann Rhem Dis 2003; 62: 1178-1184. .
 
3.
Robertson LP, Davis MJ. A longitudinal study of disease activity and functional status in a hospital cohort of patients with ankylosing spondylitis. Rheumatology (Oxford) 2004; 43: 1565-1568. .
 
4.
Elewaut D, Matucci-Cerinic M. Treatment of ankylosing spondylitis and extra-articular manifestations in everyday rheumatology practice. Rheumatology (Oxford) 2009; 48: 1029-1035. .
 
5.
Stolwijk C, van Tubergen A, Castillo-Ortiz JD, et al. Prevalence of extra-articular manifestation in patients with ankylosing spondylitis: a systematic review and meta-analysis. Ann Rhem Dis 2013 Sept. doi:10.1136/annrheumdis-2013-203582. .
 
6.
Rudwaleit M, van der Heijde D, Landewe R, et al. The development of Assessment of SpondyloArthritis International Society classification criteria for axial spondyloarthritis (part II): validation and final selection. Ann Rheum Dis 2009; 68: 777-83. .
 
7.
Van Praet L, Jans L, Carron P, et al. Degree of bone marrow oedema in sacroiliac joints of patients with axial spondyloarthritis is linked to gut inflammation and male sex: results from the GIANT cohort. Ann Rheum Dis 2014; 73: 1186-1189. .
 
8.
Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev 2014; 13: 546-549. .
 
9.
Costello ME, Elewaut D, Kenna TJ, et al. Microbes, the gut and ankylosing spondylitis. Arthritis Res Ther 2013; 15: 214. .
 
10.
Zeidler H, Hudson AP. New insights into Chlamydia and arthritis. Promise of a cure? Ann Rheum Dis 2014; 73: 637-644. .
 
11.
Ge S, He Q, Granfors K. HLA-B27 modulates intracellular growth of Salmonella pathogenicity island 2 mutants and production of cytokines in infected monocytic U937 cells. PloS ONE 2012; 7: e34093. .
 
12.
Cocchiaro JL, Valdivia RH. New insights into Chlamydia intracellular survial mechanisms. Cell Microbiol 2009; 11: 1571-1578. .
 
13.
Berthelot JM, de la Cochetiere MF, Potel G, et al. Evidence supporting a role for dormant bacteria in the pathogenesis of spondyloarthritis. Joint Bone Spine 2013; 80: 135-140. .
 
14.
Gerard HC, Stanich JA, Whittum-Hudson JA, et al. Chlamydia-associated arthritis have ocular (trachoma), not genital, serovars of C. trachomatis in synovial tissue. Microb Pathog 2010; 48: 62-68. .
 
15.
Carter JD, Inman RD. Chlamydia-induced reactive arthritis: hidden in plain sight? Best Pract Res Clin Rheumatol 2011; 25: 359-374. .
 
16.
Carter JD. Bacterial agents in spondyloarthritis; a destiny from diversity? Best Pract Res Clin Rheumatol 2010; 24: 701-714. .
 
17.
Wenink MH, Santegoets KCM, Butcher J, et al. Impaired dendritic cell proinflammatory cytokine production in psoriatic arthritis. Arthritis Rheum 2011; 63: 3313-3322. .
 
18.
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: 777-784. .
 
19.
Eppinga H, Konstantinov SR, Peppelenbosch MP, et al. The microbiome and psoriatic arthritis. Curr Rheumatol Rep 2014; 16: 407. .
 
20.
Baker PI, Love DR, Ferguson LR. Role of gut microbiota in Crohn’s disease. Expert Rev Gastroenterol Hepatol 2009; 3: 535-546. .
 
21.
Kosiewicz MM, Zirnheld AL, Alard P. Gut microbiota, immunity, and disease: a complex relationship. Front Microbiol 2011; 2: 180. .
 
22.
Strzępa A, Szczepanik M. Wpływ naturalnej flory jelitowej na odpowiedź immunologiczną. Postępy Hig Med Dośw 2013; 67: 908-920. .
 
23.
Korecka A, Arulampalam V. The gut microbiome: scourge, sentinel or spectator? J Oral Microbiol 2012; 4: 9367. .
 
24.
Lopetuso LR, Scaldaferri F, Petito V, et al. Commensal Clostridia: leading players in the maintenance of gut homeostasis. Gut Pathogens 2013; 5: 23. .
 
25.
Khosravi A, Mazmanian SK. Disruption of the gut microbiome as a risk factor for microbial infections. Curr Opin Microbiol 2013; 16: 221-227. .
 
26.
Nutsch KM, Hsieh CS. T cell tolerance and immunity to commensal bacteria. Curr Opin Immunol 2012; 24: 385-391. .
 
27.
Schaeverbeke T, Truchetet ME, Richez Ch. Gut metagenome and spondyloarthritis. Joint Bone Spine 2013; 80: 349-352. .
 
28.
Arumugam M, Raes J, Pelletier E, et al. Enterotypes of the human gut microbiome. Nature 2011; 473: 174-180. .
 
29.
Stebbings S, Munro K, Simon MA, et al. Comparison of the faecal microflora of patients with ankylosing spondylitis and controls using molecular methods of analysis. Rheumatology (Oxford) 2002; 41: 1395-1401. .
 
30.
Gibson G. Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis. FEMS Microbiol Lett 1991; 86: 103-111. .
 
31.
Stebbings SM, Taylor C, Tannock GW, et al. The immune response to autologous bacteroides in ankylosing spondylitis is characterized by reduced interleukin 10 production. J Rheumatol 2009; 36: 797-800. .
 
32.
Rosenbaum JT, Davey MP. Hypothesis: time for a gut check: HLAB27 predisposes to ankylosing spondylitis by altering the microbiome. Arthritis Rheum 2011; 63: 3195-3198. .
 
33.
Pearson C, Uhlig HH, Powrie F. Lymphoid microenvironments and innate lymphoid cells in the gut. Trends Immunol 2012; 33: 289-295. .
 
34.
Wallace KL, Zheng LB, Kanazawa Y, et al. Immunopathology of inflammatory bowel disease. World J Gastroenterol 2014; 20: 6-21. .
 
35.
Van Praet L, Jacques P, Van den Bosch F, et al. The transition of acute to chronic bowel inflammation in spondyloarthritis. Nat Rev Rheumat 2012; 8: 288-295. .
 
36.
Cherrier M, Ohnmacht C, Cording S, et al. Development and function of intestinal innate lymphoid cells. Curr Opin Immunol 2012; 24: 277-283. .
 
37.
Saltzman NH, Hung K, Haribhai D, et al. Enteric defensins are essential regulators of intestinal microbial ecology. Nat Immunol 2010; 11: 76-82. .
 
38.
Yeoh N, Burton JP, Suppiah P, et al. The role of the microbiome in rheumatic diseases. Curr Rheumatol Rep 2013; 15: 314. .
 
39.
Orlando A, Renna S, Perricone G, et al. Gastrointestinal lesions associated with spondyloarthropathies. World J Gastroenterol 2009; 15: 2443-2448. .
 
40.
Landers CJ, Cohavy O, Misra R, et al. Selected loss of tolerance evidenced by Crohn’s disease-associated immune responses to auto- and microbial antigens. Gastroenterology 2002; 123: 689-699. .
 
41.
Wallis D, Asaduzzaman A, Weisman M, et al. Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observational study. Arthritis Res Ther 2013; 15: R166. .
 
42.
Ciccia F, Alessandro R, Rizzo A, et al. Macrophage phenotype in subclinical gut inflammation of patients with ankylosing spondylitis. Rheumatology (Oxford) 2014; 53: 104-113. .
 
43.
Kenna TJ, Davidson SI, Duan R, et al. Enrichment of circulating interleukin-17-secreting interleukin-23 receptor positive gamma/delta T cells in patients with active ankylosing spondylitis. Arthritis Rheum 2012; 64: 1420-1429. .
 
44.
Roark CL, French JD, Taylor MA, et al. Exacerbation of collagen-induced arthritis by oligoclonal, IL-17-producing gamma delta T cells. J Immunol 2007; 179: 5576-5583. .
 
45.
Nanno M, Kanari Y, Naito T, et al. Exacerbating role of gamma delta T cells in chronic colitis of T-cell receptor alpha mutant mice. Gastroenterology 2008; 134: 481-490. .
 
46.
Ciccia F, Accardo-Palumbo A, Alessandro R, et al. Interleukin-22 and interleukin-22-producing NKp44+ natural killer cells in subclinical gut inflammation in ankylosing spondylitis. Arthritis Rheum 2012; 64: 1869-1878. .
 
47.
Ciccia F, Rizzo A, Accardo-Palumbo A, et al. Increased expression of interleukin-32 in the inflamed ileum of ankylosing spondylitis patients. Rheumatology (Oxford) 2012; 51: 1966-1972. .
 
48.
Fantini MC, Pallone F, Monteleone G. Common immunologic mechanisms in inflammatory bowel disease and spondyloarthropathies. World J Gastroenterol 2009; 15: 2472-2478. .
 
49.
Brakenhoff LK, van der Heijde DM, Hommes DW, et al. The joint-gut axis in inflammatory bowel diseases. J Crohns Colitis 2010; 4: 257-268. .
 
50.
Berer K, Boziki M, Kirshnamoorthy G. Selective accumulation of pro-inflammatory T cells in the intestine contributes to the resistance to autoimmune demyelinating disease. PLoS ONE 2014; 9: e8776.
 
Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
eISSN:2084-9834
ISSN:0034-6233
Journals System - logo
Scroll to top