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Erschienen in: Rheumatology International 4/2016

01.04.2016 | Review Article - Pathogenic Review

Gut inflammation and microbiome in spondyloarthritis

verfasst von: Jayakanthan Kabeerdoss, Pulukool Sandhya, Debashish Danda

Erschienen in: Rheumatology International | Ausgabe 4/2016

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Abstract

Spondyloarthritis (SpA) is chronic inflammatory disease involving joints and the spine. Bowel inflammation is common in SpA, which may be classified as acute or chronic. Chronic gut inflammation is most common in SpA patients with axial involvement as compared to those presenting with peripheral involvement alone. The pathogenesis of gut inflammation in SpA could be explained by two factors—over-activation of immunological cells and altered gut microbiome. This is exemplified by SpA animal models, namely HLA-B27-expressing transgenic animals and SKG mice models. Immunological mechanisms include homing of activated T cells from gut into synovium, excess pro-inflammatory cytokines secretion by immune cells such as IL-23 and genetic variations in immunological genes. The evidence for role of gut microbiome in SpA is gradually emerging. Recently, metagenomic study of gut microbiome by sequencing of microbial nucleic acids has enabled identification of new microbial taxa and their functions in gut of patients with SpA. In SpA, the gut microbiome could emerge as diagnostic and prognostic marker of disease. Modulation of gut microbiome is slated to have therapeutic potential as well.
Literatur
3.
Zurück zum Zitat Mielants H, De Vos M, Cuvelier C, Veys EM (1996) The role of gut inflammation in the pathogenesis of spondyloarthropathies. Acta Clin Belg 51:340–349PubMed Mielants H, De Vos M, Cuvelier C, Veys EM (1996) The role of gut inflammation in the pathogenesis of spondyloarthropathies. Acta Clin Belg 51:340–349PubMed
4.
Zurück zum Zitat Mielants H, Veys EM, Cuvelier C et al (1995) The evolution of spondyloarthropathies in relation to gut histology. II. Histological aspects. J Rheumatol 22:2273–2278PubMed Mielants H, Veys EM, Cuvelier C et al (1995) The evolution of spondyloarthropathies in relation to gut histology. II. Histological aspects. J Rheumatol 22:2273–2278PubMed
5.
Zurück zum Zitat de Vlam K, Mielants H, Cuvelier C et al (2000) Spondyloarthropathy is underestimated in inflammatory bowel disease: prevalence and HLA association. J Rheumatol 27:2860–2865PubMed de Vlam K, Mielants H, Cuvelier C et al (2000) Spondyloarthropathy is underestimated in inflammatory bowel disease: prevalence and HLA association. J Rheumatol 27:2860–2865PubMed
6.
Zurück zum Zitat De Vos M, Mielants H, Cuvelier C et al (1996) Long-term evolution of gut inflammation in patients with spondyloarthropathy. Gastroenterology 110:1696–1703PubMedCrossRef De Vos M, Mielants H, Cuvelier C et al (1996) Long-term evolution of gut inflammation in patients with spondyloarthropathy. Gastroenterology 110:1696–1703PubMedCrossRef
7.
Zurück zum Zitat Scarpa R, Manguso F, D’Arienzo A et al (2000) Microscopic inflammatory changes in colon of patients with both active psoriasis and psoriatic arthritis without bowel symptoms. J Rheumatol 27:1241–1246PubMed Scarpa R, Manguso F, D’Arienzo A et al (2000) Microscopic inflammatory changes in colon of patients with both active psoriasis and psoriatic arthritis without bowel symptoms. J Rheumatol 27:1241–1246PubMed
8.
Zurück zum Zitat Schatteman L, Mielants H, Veys EM et al (1995) Gut inflammation in psoriatic arthritis: a prospective ileocolonoscopic study. J Rheumatol 22:680–683PubMed Schatteman L, Mielants H, Veys EM et al (1995) Gut inflammation in psoriatic arthritis: a prospective ileocolonoscopic study. J Rheumatol 22:680–683PubMed
9.
Zurück zum Zitat Goel R, Danda D, Avinash B et al (2013) Clinico-pathological correlation of non specific inflammation in bowel histology with joint manifestation in a tertiary center in South India. Rheumatol Int 33:2149–2152. doi:10.1007/s00296-011-2332-x PubMedCrossRef Goel R, Danda D, Avinash B et al (2013) Clinico-pathological correlation of non specific inflammation in bowel histology with joint manifestation in a tertiary center in South India. Rheumatol Int 33:2149–2152. doi:10.​1007/​s00296-011-2332-x PubMedCrossRef
11.
Zurück zum Zitat Praet LV, Jans L, Carron P et al (2014) 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 73:1186–1189. doi:10.1136/annrheumdis-2013-203854 PubMedCrossRef Praet LV, Jans L, Carron P et al (2014) 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 73:1186–1189. doi:10.​1136/​annrheumdis-2013-203854 PubMedCrossRef
12.
Zurück zum Zitat Picco P, Gattorno M, Marchese N et al (2000) Increased gut permeability in juvenile chronic arthritides. A multivariate analysis of the diagnostic parameters. Clin Exp Rheumatol 18:773–778PubMed Picco P, Gattorno M, Marchese N et al (2000) Increased gut permeability in juvenile chronic arthritides. A multivariate analysis of the diagnostic parameters. Clin Exp Rheumatol 18:773–778PubMed
13.
Zurück zum Zitat Mielants H, Veys EM, Cuvelier C et al (1993) Gut inflammation in children with late onset pauciarticular juvenile chronic arthritis and evolution to adult spondyloarthropathy—a prospective study. J Rheumatol 20:1567–1572PubMed Mielants H, Veys EM, Cuvelier C et al (1993) Gut inflammation in children with late onset pauciarticular juvenile chronic arthritis and evolution to adult spondyloarthropathy—a prospective study. J Rheumatol 20:1567–1572PubMed
19.
23.
Zurück zum Zitat Salmi M, Rajala P, Jalkanen S (1997) Homing of mucosal leukocytes to joints. Distinct endothelial ligands in synovium mediate leukocyte-subtype specific adhesion. J Clin Invest 99:2165–2172PubMedPubMedCentralCrossRef Salmi M, Rajala P, Jalkanen S (1997) Homing of mucosal leukocytes to joints. Distinct endothelial ligands in synovium mediate leukocyte-subtype specific adhesion. J Clin Invest 99:2165–2172PubMedPubMedCentralCrossRef
24.
29.
Zurück zum Zitat Ciccia F, Bombardieri M, Principato A et al (2009) Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis. Arthritis Rheum 60:955–965. doi:10.1002/art.24389 PubMedCrossRef Ciccia F, Bombardieri M, Principato A et al (2009) Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis. Arthritis Rheum 60:955–965. doi:10.​1002/​art.​24389 PubMedCrossRef
30.
Zurück zum Zitat Gheita TA, El Gazzar II, El-Fishawy HS et al (2014) Involvement of IL-23 in enteropathic arthritis patients with inflammatory bowel disease: preliminary results. Clin Rheumatol 33:713–717. doi:10.1007/s10067-013-2469-y PubMed Gheita TA, El Gazzar II, El-Fishawy HS et al (2014) Involvement of IL-23 in enteropathic arthritis patients with inflammatory bowel disease: preliminary results. Clin Rheumatol 33:713–717. doi:10.​1007/​s10067-013-2469-y PubMed
31.
Zurück zum Zitat Sherlock JP, Joyce-Shaikh B, Turner SP et al (2012) IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+ CD4−CD8− entheseal resident T cells. Nat Med 18:1069–1076. doi:10.1038/nm.2817 PubMedCrossRef Sherlock JP, Joyce-Shaikh B, Turner SP et al (2012) IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+ CD4−CD8− entheseal resident T cells. Nat Med 18:1069–1076. doi:10.​1038/​nm.​2817 PubMedCrossRef
36.
Zurück zum Zitat Ciccia F, Accardo-Palumbo A, Giardina A et al (2010) Expansion of intestinal CD4+ CD25high Treg cells in patients with ankylosing spondylitis: a putative role for interleukin-10 in preventing intestinal Th17 response. Arthritis Rheum 62:3625–3634. doi:10.1002/art.27699 PubMedCrossRef Ciccia F, Accardo-Palumbo A, Giardina A et al (2010) Expansion of intestinal CD4+ CD25high Treg cells in patients with ankylosing spondylitis: a putative role for interleukin-10 in preventing intestinal Th17 response. Arthritis Rheum 62:3625–3634. doi:10.​1002/​art.​27699 PubMedCrossRef
37.
Zurück zum Zitat Ciccia F, Accardo-Palumbo A, Alessandro R et al (2012) Interleukin-22 and interleukin-22-producing NKp44+ natural killer cells in subclinical gut inflammation in ankylosing spondylitis. Arthritis Rheum 64:1869–1878. doi:10.1002/art.34355 PubMedCrossRef Ciccia F, Accardo-Palumbo A, Alessandro R et al (2012) Interleukin-22 and interleukin-22-producing NKp44+ natural killer cells in subclinical gut inflammation in ankylosing spondylitis. Arthritis Rheum 64:1869–1878. doi:10.​1002/​art.​34355 PubMedCrossRef
43.
44.
Zurück zum Zitat Ciccia F, Guggino G, Rizzo A et al (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. Ann Rheum Dis. doi:10.1136/annrheumdis-2014-206323 PubMed Ciccia F, Guggino G, Rizzo A et al (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. Ann Rheum Dis. doi:10.​1136/​annrheumdis-2014-206323 PubMed
49.
Zurück zum Zitat Poeck H, Bscheider M, Gross O et al (2010) Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production. Nat Immunol 11:63–69. doi:10.1038/ni.1824 PubMedCrossRef Poeck H, Bscheider M, Gross O et al (2010) Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production. Nat Immunol 11:63–69. doi:10.​1038/​ni.​1824 PubMedCrossRef
50.
54.
Zurück zum Zitat Rastall RA (2004) Bacteria in the gut: friends and foes and how to alter the balance. J Nutr 134:2022S–2026SPubMed Rastall RA (2004) Bacteria in the gut: friends and foes and how to alter the balance. J Nutr 134:2022S–2026SPubMed
57.
58.
Zurück zum Zitat Taurog JD, Richardson JA, Croft JT et al (1994) The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med 180:2359–2364PubMedCrossRef Taurog JD, Richardson JA, Croft JT et al (1994) The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med 180:2359–2364PubMedCrossRef
59.
Zurück zum Zitat Rath HC, Herfarth HH, Ikeda JS et al (1996) Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis, and arthritis in HLA-B27/human beta2 microglobulin transgenic rats. J Clin Invest 98:945–953. doi:10.1172/JCI118878 PubMedPubMedCentralCrossRef Rath HC, Herfarth HH, Ikeda JS et al (1996) Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis, and arthritis in HLA-B27/human beta2 microglobulin transgenic rats. J Clin Invest 98:945–953. doi:10.​1172/​JCI118878 PubMedPubMedCentralCrossRef
61.
Zurück zum Zitat Onderdonk AB, Richardson JA, Hammer RE, Taurog JD (1998) Correlation of cecal microflora of HLA-B27 transgenic rats with inflammatory bowel disease. Infect Immun 66:6022–6023PubMedPubMedCentral Onderdonk AB, Richardson JA, Hammer RE, Taurog JD (1998) Correlation of cecal microflora of HLA-B27 transgenic rats with inflammatory bowel disease. Infect Immun 66:6022–6023PubMedPubMedCentral
64.
Zurück zum Zitat Rath HC (2002) Role of commensal bacteria in chronic experimental colitis: lessons from the HLA-B27 transgenic rat. Pathobiol J Immunopathol Mol Cell Biol 70:131–138CrossRef Rath HC (2002) Role of commensal bacteria in chronic experimental colitis: lessons from the HLA-B27 transgenic rat. Pathobiol J Immunopathol Mol Cell Biol 70:131–138CrossRef
65.
Zurück zum Zitat Png CW, Lindén SK, Gilshenan KS et al (2010) Mucolytic bacteria with increased prevalence in IBD mucosa augment in vitro utilization of mucin by other bacteria. Am J Gastroenterol 105:2420–2428. doi:10.1038/ajg.2010.281 PubMedCrossRef Png CW, Lindén SK, Gilshenan KS et al (2010) Mucolytic bacteria with increased prevalence in IBD mucosa augment in vitro utilization of mucin by other bacteria. Am J Gastroenterol 105:2420–2428. doi:10.​1038/​ajg.​2010.​281 PubMedCrossRef
66.
Zurück zum Zitat Reháková Z, Capková J, Stĕpánková R et al (2000) Germ-free mice do not develop ankylosing enthesopathy, a spontaneous joint disease. Hum Immunol 61:555–558PubMedCrossRef Reháková Z, Capková J, Stĕpánková R et al (2000) Germ-free mice do not develop ankylosing enthesopathy, a spontaneous joint disease. Hum Immunol 61:555–558PubMedCrossRef
70.
Zurück zum Zitat Sakaguchi S, Takahashi T, Hata H et al (2006) SKG mice, a monogenic model of autoimmune arthritis due to altered signal transduction in T-cells. In: Holmdahl R (ed) Hered. Basis Rheum. Dis. Birkhäuser Basel, pp 147–159 Sakaguchi S, Takahashi T, Hata H et al (2006) SKG mice, a monogenic model of autoimmune arthritis due to altered signal transduction in T-cells. In: Holmdahl R (ed) Hered. Basis Rheum. Dis. Birkhäuser Basel, pp 147–159
71.
72.
Zurück zum Zitat Benham H, Rehaume LM, Hasnain SZ et al (2014) Interleukin-23 mediates the intestinal response to microbial β-1,3-glucan and the development of spondyloarthritis pathology in SKG mice. Arthritis Rheumatol Hoboken NJ 66:1755–1767. doi:10.1002/art.38638 CrossRef Benham H, Rehaume LM, Hasnain SZ et al (2014) Interleukin-23 mediates the intestinal response to microbial β-1,3-glucan and the development of spondyloarthritis pathology in SKG mice. Arthritis Rheumatol Hoboken NJ 66:1755–1767. doi:10.​1002/​art.​38638 CrossRef
73.
Zurück zum Zitat Akramiene D, Kondrotas A, Didziapetriene J, Kevelaitis E (2007) Effects of beta-glucans on the immune system. Med Kaunas Lith 43:597–606 Akramiene D, Kondrotas A, Didziapetriene J, Kevelaitis E (2007) Effects of beta-glucans on the immune system. Med Kaunas Lith 43:597–606
74.
Zurück zum Zitat Rehaume LM, Mondot S, Aguirre de Cárcer D et al (2014) ZAP-70 genotype disrupts the relationship between microbiota and host, leading to spondyloarthritis and ileitis in SKG mice. Arthritis Rheumatol Hoboken NJ 66:2780–2792. doi:10.1002/art.38773 CrossRef Rehaume LM, Mondot S, Aguirre de Cárcer D et al (2014) ZAP-70 genotype disrupts the relationship between microbiota and host, leading to spondyloarthritis and ileitis in SKG mice. Arthritis Rheumatol Hoboken NJ 66:2780–2792. doi:10.​1002/​art.​38773 CrossRef
75.
76.
Zurück zum Zitat Stebbings S, Munro K, Simon MA et al (2002) Comparison of the faecal microflora of patients with ankylosing spondylitis and controls using molecular methods of analysis. Rheumatol Oxf Engl 41:1395–1401CrossRef Stebbings S, Munro K, Simon MA et al (2002) Comparison of the faecal microflora of patients with ankylosing spondylitis and controls using molecular methods of analysis. Rheumatol Oxf Engl 41:1395–1401CrossRef
78.
Zurück zum Zitat Ebringer A, Wilson C (1996) The use of a low starch diet in the treatment of patients suffering from ankylosing spondylitis. Clin Rheumatol 15(Suppl 1):62–66PubMedCrossRef Ebringer A, Wilson C (1996) The use of a low starch diet in the treatment of patients suffering from ankylosing spondylitis. Clin Rheumatol 15(Suppl 1):62–66PubMedCrossRef
79.
Zurück zum Zitat Rashid T, Ebringer A (2011) Gut-mediated and HLA-B27-associated arthritis: an emphasis on ankylosing spondylitis and Crohn’s disease with a proposal for the use of new treatment. Discov Med 12:187–194PubMed Rashid T, Ebringer A (2011) Gut-mediated and HLA-B27-associated arthritis: an emphasis on ankylosing spondylitis and Crohn’s disease with a proposal for the use of new treatment. Discov Med 12:187–194PubMed
80.
Zurück zum Zitat Stone MA, Payne U, Schentag C et al (2004) Comparative immune responses to candidate arthritogenic bacteria do not confirm a dominant role for Klebsiella pneumonia in the pathogenesis of familial ankylosing spondylitis. Rheumatol Oxf Engl 43:148–155. doi:10.1093/rheumatology/keg482 CrossRef Stone MA, Payne U, Schentag C et al (2004) Comparative immune responses to candidate arthritogenic bacteria do not confirm a dominant role for Klebsiella pneumonia in the pathogenesis of familial ankylosing spondylitis. Rheumatol Oxf Engl 43:148–155. doi:10.​1093/​rheumatology/​keg482 CrossRef
82.
Zurück zum Zitat Wallis D, Asaduzzaman A, Weisman M et al (2013) Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observational study. Arthritis Res Ther 15:R166. doi:10.1186/ar4350 PubMedPubMedCentralCrossRef Wallis D, Asaduzzaman A, Weisman M et al (2013) Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observational study. Arthritis Res Ther 15:R166. doi:10.​1186/​ar4350 PubMedPubMedCentralCrossRef
84.
Zurück zum Zitat Kabeerdoss J, Jayakanthan P, Pugazhendhi S, Ramakrishna BS (2015) Alterations of mucosal microbiota in the colon of patients with inflammatory bowel disease revealed by real time polymerase chain reaction amplification of 16S ribosomal ribonucleic acid. Indian J Med Res 142:23–32. doi:10.4103/0971-5916.162091 PubMedPubMedCentral Kabeerdoss J, Jayakanthan P, Pugazhendhi S, Ramakrishna BS (2015) Alterations of mucosal microbiota in the colon of patients with inflammatory bowel disease revealed by real time polymerase chain reaction amplification of 16S ribosomal ribonucleic acid. Indian J Med Res 142:23–32. doi:10.​4103/​0971-5916.​162091 PubMedPubMedCentral
85.
Zurück zum Zitat Scher JU, Ubeda C, Artacho A et al (2015) Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheumatol Hoboken NJ 67:128–139. doi:10.1002/art.38892 CrossRef Scher JU, Ubeda C, Artacho A et al (2015) Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheumatol Hoboken NJ 67:128–139. doi:10.​1002/​art.​38892 CrossRef
87.
Zurück zum Zitat Siala M, Jaulhac B, Gdoura R et al (2008) Analysis of bacterial DNA in synovial tissue of Tunisian patients with reactive and undifferentiated arthritis by broad-range PCR, cloning and sequencing. Arthritis Res Ther 10:R40. doi:10.1186/ar2398 PubMedPubMedCentralCrossRef Siala M, Jaulhac B, Gdoura R et al (2008) Analysis of bacterial DNA in synovial tissue of Tunisian patients with reactive and undifferentiated arthritis by broad-range PCR, cloning and sequencing. Arthritis Res Ther 10:R40. doi:10.​1186/​ar2398 PubMedPubMedCentralCrossRef
88.
Zurück zum Zitat Siala M, Gdoura R, Fourati H et al (2009) Broad-range PCR, cloning and sequencing of the full 16S rRNA gene for detection of bacterial DNA in synovial fluid samples of Tunisian patients with reactive and undifferentiated arthritis. Arthritis Res Ther 11:R102. doi:10.1186/ar2748 PubMedPubMedCentralCrossRef Siala M, Gdoura R, Fourati H et al (2009) Broad-range PCR, cloning and sequencing of the full 16S rRNA gene for detection of bacterial DNA in synovial fluid samples of Tunisian patients with reactive and undifferentiated arthritis. Arthritis Res Ther 11:R102. doi:10.​1186/​ar2748 PubMedPubMedCentralCrossRef
89.
93.
Zurück zum Zitat Baharav E, Mor F, Halpern M, Weinberger A (2004) Lactobacillus GG bacteria ameliorate arthritis in lewis rats. J Nutr 134:1964–1969PubMed Baharav E, Mor F, Halpern M, Weinberger A (2004) Lactobacillus GG bacteria ameliorate arthritis in lewis rats. J Nutr 134:1964–1969PubMed
95.
Zurück zum Zitat Magrone T, Jirillo E (2014) The interleukin-17/interleukin-22 innate axis in the gut as a new drug target in allergic-inflammatory and autoimmune diseases. A working hypothesis. Endocr Metab Immune Disord Drug Targets 14:145–151PubMedCrossRef Magrone T, Jirillo E (2014) The interleukin-17/interleukin-22 innate axis in the gut as a new drug target in allergic-inflammatory and autoimmune diseases. A working hypothesis. Endocr Metab Immune Disord Drug Targets 14:145–151PubMedCrossRef
96.
97.
Zurück zum Zitat Dieleman LA, Goerres MS, Arends A et al (2003) Lactobacillus GG prevents recurrence of colitis in HLA-B27 transgenic rats after antibiotic treatment. Gut 52:370–376PubMedPubMedCentralCrossRef Dieleman LA, Goerres MS, Arends A et al (2003) Lactobacillus GG prevents recurrence of colitis in HLA-B27 transgenic rats after antibiotic treatment. Gut 52:370–376PubMedPubMedCentralCrossRef
100.
Zurück zum Zitat Sanges M, Valente G, Rea M et al (2009) Probiotics in spondyloarthropathy associated with ulcerative colitis: a pilot study. Eur Rev Med Pharmacol Sci 13:233–234PubMed Sanges M, Valente G, Rea M et al (2009) Probiotics in spondyloarthropathy associated with ulcerative colitis: a pilot study. Eur Rev Med Pharmacol Sci 13:233–234PubMed
102.
Zurück zum Zitat Kleessen B, Hartmann L, Blaut M (2001) Oligofructose and long-chain inulin: influence on the gut microbial ecology of rats associated with a human faecal flora. Br J Nutr 86:291–300PubMedCrossRef Kleessen B, Hartmann L, Blaut M (2001) Oligofructose and long-chain inulin: influence on the gut microbial ecology of rats associated with a human faecal flora. Br J Nutr 86:291–300PubMedCrossRef
105.
Zurück zum Zitat Kanauchi O, Suga T, Tochihara M et al (2013) Treatment of ulcerative colitis by feeding with germinated barley foodstuff: first report of a multicenter open control trial. J Gastroenterol 37:67–72. doi:10.1007/BF03326417 CrossRef Kanauchi O, Suga T, Tochihara M et al (2013) Treatment of ulcerative colitis by feeding with germinated barley foodstuff: first report of a multicenter open control trial. J Gastroenterol 37:67–72. doi:10.​1007/​BF03326417 CrossRef
106.
Zurück zum Zitat Scaldaferri F, Gerardi V, Lopetuso LR et al (2013) Gut microbial flora, prebiotics, and probiotics in IBD: their current usage and utility. BioMed Res Int 2013:e435268. doi:10.1155/2013/435268 CrossRef Scaldaferri F, Gerardi V, Lopetuso LR et al (2013) Gut microbial flora, prebiotics, and probiotics in IBD: their current usage and utility. BioMed Res Int 2013:e435268. doi:10.​1155/​2013/​435268 CrossRef
107.
Zurück zum Zitat Hoentjen F, Welling GW, Harmsen HJM et al (2005) Reduction of colitis by prebiotics in HLA-B27 transgenic rats is associated with microflora changes and immunomodulation. Inflamm Bowel Dis 11:977–985PubMedCrossRef Hoentjen F, Welling GW, Harmsen HJM et al (2005) Reduction of colitis by prebiotics in HLA-B27 transgenic rats is associated with microflora changes and immunomodulation. Inflamm Bowel Dis 11:977–985PubMedCrossRef
110.
111.
Zurück zum Zitat Frydén A, Bengtsson A, Foberg U et al (1990) Early antibiotic treatment of reactive arthritis associated with enteric infections: clinical and serological study. BMJ 301:1299–1302PubMedPubMedCentralCrossRef Frydén A, Bengtsson A, Foberg U et al (1990) Early antibiotic treatment of reactive arthritis associated with enteric infections: clinical and serological study. BMJ 301:1299–1302PubMedPubMedCentralCrossRef
112.
Zurück zum Zitat Rohekar S, Chan J, Tse SML et al (2015) 2014 Update of the Canadian Rheumatology Association/Spondyloarthritis Research Consortium of Canada Treatment Recommendations for the management of spondyloarthritis. Part II: specific management recommendations. J Rheumatol 42:654–664. doi:10.3899/jrheum.141001 PubMedCrossRef Rohekar S, Chan J, Tse SML et al (2015) 2014 Update of the Canadian Rheumatology Association/Spondyloarthritis Research Consortium of Canada Treatment Recommendations for the management of spondyloarthritis. Part II: specific management recommendations. J Rheumatol 42:654–664. doi:10.​3899/​jrheum.​141001 PubMedCrossRef
114.
Zurück zum Zitat Eiseman B, Silen W, Bascom GS, Kauvar AJ (1958) Fecal enema as an adjunct in the treatment of pseudomembranous enterocolitis. Surgery 44:854–859PubMed Eiseman B, Silen W, Bascom GS, Kauvar AJ (1958) Fecal enema as an adjunct in the treatment of pseudomembranous enterocolitis. Surgery 44:854–859PubMed
116.
Zurück zum Zitat Smith MB, Kelly C, Alm EJ (2014) Policy: how to regulate faecal transplants. Nature 506:290–291PubMedCrossRef Smith MB, Kelly C, Alm EJ (2014) Policy: how to regulate faecal transplants. Nature 506:290–291PubMedCrossRef
120.
Zurück zum Zitat Uk, IBD Genetics Consortium, Barrett JC, Lee JC et al (2009) Genome-wide association study of ulcerative colitis identifies three new susceptibility loci, including the HNF4A region. Nat Genet 41:1330–1334. doi:10.1038/ng.483 CrossRef Uk, IBD Genetics Consortium, Barrett JC, Lee JC et al (2009) Genome-wide association study of ulcerative colitis identifies three new susceptibility loci, including the HNF4A region. Nat Genet 41:1330–1334. doi:10.​1038/​ng.​483 CrossRef
121.
123.
Zurück zum Zitat Evans DM, Spencer CCA, Pointon JJ et al (2011) Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. Nat Genet 43:761–767. doi:10.1038/ng.873 PubMedPubMedCentralCrossRef Evans DM, Spencer CCA, Pointon JJ et al (2011) Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. Nat Genet 43:761–767. doi:10.​1038/​ng.​873 PubMedPubMedCentralCrossRef
124.
Zurück zum Zitat Wellcome Trust Case Control Consortium (2007) Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 447:661–678. doi:10.1038/nature05911 CrossRef Wellcome Trust Case Control Consortium (2007) Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 447:661–678. doi:10.​1038/​nature05911 CrossRef
125.
Zurück zum Zitat Australo-Anglo-American Spondyloarthritis Consortium (TASC), Reveille JD, Sims A-M et al (2010) Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci. Nat Genet 42:123–127. doi:10.1038/ng.513 CrossRef Australo-Anglo-American Spondyloarthritis Consortium (TASC), Reveille JD, Sims A-M et al (2010) Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci. Nat Genet 42:123–127. doi:10.​1038/​ng.​513 CrossRef
129.
134.
Zurück zum Zitat Yang S-K, Hong M, Zhao W et al (2014) Genome-wide association study of Crohn’s disease in Koreans revealed three new susceptibility loci and common attributes of genetic susceptibility across ethnic populations. Gut 63:80–87. doi:10.1136/gutjnl-2013-305193 PubMedCrossRef Yang S-K, Hong M, Zhao W et al (2014) Genome-wide association study of Crohn’s disease in Koreans revealed three new susceptibility loci and common attributes of genetic susceptibility across ethnic populations. Gut 63:80–87. doi:10.​1136/​gutjnl-2013-305193 PubMedCrossRef
Metadaten
Titel
Gut inflammation and microbiome in spondyloarthritis
verfasst von
Jayakanthan Kabeerdoss
Pulukool Sandhya
Debashish Danda
Publikationsdatum
01.04.2016
Verlag
Springer Berlin Heidelberg
Erschienen in
Rheumatology International / Ausgabe 4/2016
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-015-3414-y

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Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

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