The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis

Inflammatory arthritis is a condition which is characterised by recurrent episodes of joint pain and swelling. It encompasses a spectrum of disorders ranging from rheumatoid arthritis to ankylosing spondylitis. In these conditions, for reasons that are poorly understood, the immune system raises an...

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Main Authors: Animesh Singh, Sarah Karrar
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/158793
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spelling doaj-c3999d046e484d77956862ba67ad894f2020-11-24T23:53:27ZengHindawi LimitedInternational Journal of Inflammation2090-80402042-00992014-01-01201410.1155/2014/158793158793The Role of Intracellular Organisms in the Pathogenesis of Inflammatory ArthritisAnimesh Singh0Sarah Karrar1Department of Rheumatology, Charing Cross Hospital, Imperial College NHS Trust, London W6 8RF, UKDepartment of Rheumatology, Charing Cross Hospital, Imperial College NHS Trust, London W6 8RF, UKInflammatory arthritis is a condition which is characterised by recurrent episodes of joint pain and swelling. It encompasses a spectrum of disorders ranging from rheumatoid arthritis to ankylosing spondylitis. In these conditions, for reasons that are poorly understood, the immune system raises an inflammatory response within the joint space. In some cases, autoantigens have been identified (e.g., anticitrullinated peptides in rheumatoid arthritis), but the absence of these, in the seronegative arthritides, for example, raises question as to the underlying pathogenesis. Interest has, therefore, turned to host-pathogen interactions and whether aberrant immune responses to these could explain the development of arthritis. This has been most widely studied in reactive arthritis (ReA), where an infectious episode precedes the development of the joint symptoms. In this review, we present the evidence for the role of host-bacterial interactions in the pathogenesis of joint inflammation with particular emphasis on ReA. We discuss a range of possible mechanisms including molecular mimicry, persistent low grade infections, and abnormal host responses to common bacterial causes of reactive arthritis as well as discussing some of the clinical challenges that we face in making the diagnosis and in treatment of persistent symptoms.http://dx.doi.org/10.1155/2014/158793
collection DOAJ
language English
format Article
sources DOAJ
author Animesh Singh
Sarah Karrar
spellingShingle Animesh Singh
Sarah Karrar
The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
International Journal of Inflammation
author_facet Animesh Singh
Sarah Karrar
author_sort Animesh Singh
title The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
title_short The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
title_full The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
title_fullStr The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
title_full_unstemmed The Role of Intracellular Organisms in the Pathogenesis of Inflammatory Arthritis
title_sort role of intracellular organisms in the pathogenesis of inflammatory arthritis
publisher Hindawi Limited
series International Journal of Inflammation
issn 2090-8040
2042-0099
publishDate 2014-01-01
description Inflammatory arthritis is a condition which is characterised by recurrent episodes of joint pain and swelling. It encompasses a spectrum of disorders ranging from rheumatoid arthritis to ankylosing spondylitis. In these conditions, for reasons that are poorly understood, the immune system raises an inflammatory response within the joint space. In some cases, autoantigens have been identified (e.g., anticitrullinated peptides in rheumatoid arthritis), but the absence of these, in the seronegative arthritides, for example, raises question as to the underlying pathogenesis. Interest has, therefore, turned to host-pathogen interactions and whether aberrant immune responses to these could explain the development of arthritis. This has been most widely studied in reactive arthritis (ReA), where an infectious episode precedes the development of the joint symptoms. In this review, we present the evidence for the role of host-bacterial interactions in the pathogenesis of joint inflammation with particular emphasis on ReA. We discuss a range of possible mechanisms including molecular mimicry, persistent low grade infections, and abnormal host responses to common bacterial causes of reactive arthritis as well as discussing some of the clinical challenges that we face in making the diagnosis and in treatment of persistent symptoms.
url http://dx.doi.org/10.1155/2014/158793
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