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      Ankylosing spondylitis: etiology, pathogenesis, and treatments

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          Abstract

          Ankylosing spondylitis (AS), a common type of spondyloarthropathy, is a chronic inflammatory autoimmune disease that mainly affects spine joints, causing severe, chronic pain; additionally, in more advanced cases, it can cause spine fusion. Significant progress in its pathophysiology and treatment has been achieved in the last decade. Immune cells and innate cytokines have been suggested to be crucial in the pathogenesis of AS, especially human leukocyte antigen (HLA)‑B27 and the interleukin‑23/17 axis. However, the pathogenesis of AS remains unclear. The current study reviewed the etiology and pathogenesis of AS, including genome-wide association studies and cytokine pathways. This study also summarized the current pharmaceutical and surgical treatment with a discussion of future potential therapies.

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          Analysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared loci

          David Ellinghaus, Luke Jostins, Sarah L Spain … (2016)
          We simultaneously investigated the genetic landscape of ankylosing spondylitis, Crohn's disease, psoriasis, primary sclerosing cholangitis and ulcerative colitis to investigate pleiotropy and the relationship between these clinically related diseases. Using high-density genotype data from more than 86,000 individuals of European-ancestry we identified 244 independent multi-disease signals including 27 novel genome-wide significant susceptibility loci and 3 unreported shared risk loci. Complex pleiotropy was supported when contrasting multi-disease signals with expression data sets from human, rat and mouse, and epigenetic and expressed enhancer profiles. The comorbidities among the five immune diseases were best explained by biological pleiotropy rather than heterogeneity (a subgroup of cases that is genetically identical to another disease, possibly due to diagnostic misclassification, molecular subtypes, or excessive comorbidity). In particular, the strong comorbidity between primary sclerosing cholangitis and inflammatory bowel disease is likely the result of a unique disease, which is genetically distinct from classical inflammatory bowel disease phenotypes.
          Article 0 comments Cited 352 times – based on 0 reviews     Review now
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            The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats

            J.L. Fernandez Puentes, JL Fernandez-Luna, WA Simmons … (1994)
            A number of inflammatory disease states occur with greatly increased frequency in individuals inheriting the human major histocompatibility complex class I allele HLA-B27. In a minority of cases, namely those with B27-associated reactive arthritis, there is good evidence that the disease state is triggered by infection with an enteric or genitourinary bacterial pathogen. For the majority of B27-associated disease, no definite pathogenetic role for bacteria has been established. However, in these latter cases intestinal inflammation can often be demonstrated, and it sometimes occupies a major part of the clinical picture. Rats transgenic for B27 are known to develop a disorder resembling B27-associated human disease, with prominent intestinal, joint, skin, and male genital inflammatory lesions. We report here that B27 transgenic rats raised in a germfree environment do not develop inflammatory intestinal or peripheral joint disease, whereas the skin and genital inflammatory lesions are unaffected by the germfree state. These findings support the concept that gut and joint inflammation are pathogenetically closely related, and they provide direct evidence that the commensal gut flora play an important role in the pathogenesis of B27-associated gut and joint inflammation.
            Article 0 comments Cited 217 times – based on 0 reviews     Review now
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              Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci.

              John Reveille, Anne-Marie Sims, Patrick Danoy … (2010)
              To identify susceptibility loci for ankylosing spondylitis, we undertook a genome-wide association study in 2,053 unrelated ankylosing spondylitis cases among people of European descent and 5,140 ethnically matched controls, with replication in an independent cohort of 898 ankylosing spondylitis cases and 1,518 controls. Cases were genotyped with Illumina HumHap370 genotyping chips. In addition to strong association with the major histocompatibility complex (MHC; P < 10(-800)), we found association with SNPs in two gene deserts at 2p15 (rs10865331; combined P = 1.9 x 10(-19)) and 21q22 (rs2242944; P = 8.3 x 10(-20)), as well as in the genes ANTXR2 (rs4333130; P = 9.3 x 10(-8)) and IL1R2 (rs2310173; P = 4.8 x 10(-7)). We also replicated previously reported associations at IL23R (rs11209026; P = 9.1 x 10(-14)) and ERAP1 (rs27434; P = 5.3 x 10(-12)). This study reports four genetic loci associated with ankylosing spondylitis risk and identifies a major role for the interleukin (IL)-23 and IL-1 cytokine pathways in disease susceptibility.
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                Author and article information

                Contributors
                Xu Cao: xcao11@jhmi.edu
                Xisheng Weng: xshweng@medmail.com.cn
                Journal
                Journal ID (nlm-ta): Bone Res
                Journal ID (iso-abbrev): Bone Res
                Title: Bone Research
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 2095-4700
                ISSN (Electronic): 2095-6231
                Publication date (Electronic): 5 August 2019
                Publication date PMC-release: 5 August 2019
                Publication date Collection: 2019
                Volume: 7
                Electronic Location Identifier: 22
                Affiliations
                [1 ]ISNI 0000 0001 0662 3178, GRID grid.12527.33, Department of Orthopedics, Peking Union Medical College Hospital, , Chinese Academy of Medical Sciences & Peking Union Medical College, ; 100730 Beijing, China
                [2 ]ISNI 0000 0001 0662 3178, GRID grid.12527.33, Department of Clinical Medicine, , Chinese Academy of Medical Sciences & Peking Union Medical College, ; 100730 Beijing, China
                [3 ]ISNI 0000 0001 0705 3621, GRID grid.240684.c, Department of Orthopedic Surgery, , Rush University Medical Center, ; Chicago, IL 60612 USA
                [4 ]ISNI 0000 0001 2171 9311, GRID grid.21107.35, Department of Orthopedic Surgery, School of Medicine, , Johns Hopkins University, ; Baltimore, MD USA
                Author information
                http://orcid.org/0000-0001-6395-706X
                Article
                Publisher ID: 57
                DOI: 10.1038/s41413-019-0057-8
                PMC ID: 6804882
                PubMed ID: 31666997
                SO-VID: f367b6e7-d8b2-4e61-b8b1-6cf055073796
                Copyright © © The Author(s) 2019
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 27 December 2018
                Date revision received : 20 May 2019
                Date accepted : 23 May 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100004826, Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation);
                Award ID: 7184325
                Award Recipient :
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                Keywords: calcium and phosphate metabolic disorders,pathogenesis
                Data availability:
                Keywords: calcium and phosphate metabolic disorders, pathogenesis

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