Evidence of Cellular Immune Response to Outer Membrane Protein of<i>Salmonella typhimurium</i>in Patients with Enthesitis-related Arthritis Subtype of Juvenile Idiopathic Arthritis

Singh, Yogesh Preet; Singh, Amit Kumatr; Aggarwal, Amita; Misra, Ramnath

doi:10.3899/jrheum.100542

Cited by 21 publications

(12 citation statements)

References 26 publications

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“…Among these 12 patients, 11 showed a proliferative response to OMP. These outer membrane proteins are accessible to the immune system and might represent a T cell-mediated target of synovial fluid and peripheral blood mononuclear cells in patients with enthesitisrelated arthritis [54].…”

Section: The Potential Role Of Bacteria In Juvenile Idiopathic Arthritismentioning

confidence: 99%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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Over the years, the commonly used term to describe juvenile idiopathic arthritis (JIA) has changed. By definition, JIA includes all types of arthritis with no apparent cause, lasting more than 6 weeks, in patients aged less than 16 years at onset. JIA pathogenesis is still poorly understood: the interaction between environmental factors and multiple genes has been proposed as the most relevant working mechanism to the development of JIA. The concept that various microbes that colonize or infect not only the mucosal surfaces, like the oral cavity, but also the airways and gut might trigger autoimmune processes, resulting in chronic arthritides, and JIA was first drafted at the outset of last century. JIA development might be initiated and sustained by the exposure to environmental factors, including infectious agents which affect people at a young age, depending on the underlying genetic predisposition to synovial inflammation. Many data from patients with JIA suggest a scenario in which different external antigens incite multiple antigen-specific pathways, cytotoxic T cell responses, activation of classical complement cascade, and production of proinflammatory cytokines. In this review, emphasis is paid not only to the potential role of parvovirus B19 and Epstein-Barr virus in primis but also to the general involvement of different bacteria as Salmonella spp., Shigella spp., Campylobacter spp., Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bartonella henselae, and Streptococcus pyogenes for the development of immune-mediated arthritides during childhood. No unequivocal evidence favoring or refuting these associations has been clearly proved, and today, the strict definition of JIA etiology remains unknown. The infection can represent a random event in a susceptible individual, or it can be a necessary factor in JIA development, always in combination with a peculiar genetic background. Further studies are needed in order to address the unsolved questions concerning this issue.

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Section: The Potential Role Of Bacteria In Juvenile Idiopathic Arthritismentioning

confidence: 99%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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“…Stoll et al demonstrated that in children with ERA [ 8 ], serum IgA against B. fragilis was directly proportional to fecal Bacteroides abundance, while controls had the opposite relationship, which they took to indicate that patients had a more pathogenic response against this organism. Additionally, Singh et al (2011) demonstrated increased T cell responses to the Salmonella outer membrane protein in ERA patients compared to controls [ 54 ].…”

Section: Mechanisms By Which the Microbiota Might Predispose To Jiamentioning

confidence: 99%

Gut microbiota-host interactions and juvenile idiopathic arthritis

et al. 2016

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BackgroundJuvenile idiopathic arthritis is the most common form of chronic arthritis in children. There is mounting evidence that the microbiota may influence the disease.Main bodyRecent observations in several systemic inflammatory diseases including JIA have indicated that abnormalities in the contents of the microbiota may be factors in disease pathogenesis, while other studies in turn have shown that environmental factors impacting the composition of the microbiota, such as delivery mode and early exposure to antibiotics, affect the risk of chronic inflammatory diseases including JIA. Microbial alterations may predispose to JIA through a variety of mechanisms, including impaired immunologic development, alterations in the balances of pro- versus anti-inflammatory bacteria, and low-grade mucosal inflammation. Additional confirmatory studies of microbiota aberrations and their risk factors are needed, as well as additional mechanistic studies linking these alterations to the disease itself.ConclusionsThe microbiota may influence the risk of JIA and other systemic inflammatory conditions through a variety of mechanisms. Additional research is required to improve our understanding of the links between the microbiota and arthritis, and the treatment implications thereof.

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“…Despite these differences, serum IgA and IgG antibody against F. prausnitzii and B. fragilis were similar between controls and patients. There is also some evidence of a cellular immune response to the outer membrane protein of Salmonella typhimurium in juvenile SpA patients compared to healthy controls [54]. Intriguingly, study of the microbiota of juvenile SpA patients revealed that patients could be stratified into two distinct clusters, one dominated by Bacteroides genus members, the other by Akkermansia muciniphila.…”

Section: Juvenile Spamentioning

confidence: 99%

The intestinal microbiome in spondyloarthritis

Gill

Asquith

Rosenbaum

et al. 2015

Current Opinion in Rheumatology

103

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Purpose of the review Microbial dysbiosis in the gut is emerging as a common component in various inflammatory disorders including spondyloarthritis (SpA). The depth of this influence has begun to be realized with next generation sequencing of the gut microbiome providing unbiased assessment of previously uncharted bacterial populations. Recent findings Decreased numbers of Firmicutes, a major phyla of gut commensals, especially the species Faecalibacterium prausnitzii and Clostridium leptum have been found in various inflammatory disorders including SpA and IBD, and could be an important link between SpA and gut inflammation. Multiple studies in ankylosing spondylitis, psoriatic arthritis, juvenile SpA and animals models of SpA are revealing common bacterial associations among these diseases as well as IBD. Summary We are beginning to appreciate the complex relationship between the gut microbiome and host immune regulation and dysregulation in health and disease. Potentially important differences have been revealed in SpA, but cause and effect relationships remain far from established. Many critical questions remain to be answered before we can apply new knowledge to improve therapeutics in SpA.

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Evidence of Cellular Immune Response to Outer Membrane Protein ofSalmonella typhimuriumin Patients with Enthesitis-related Arthritis Subtype of Juvenile Idiopathic Arthritis

Cited by 21 publications

References 26 publications

The Etiology of Juvenile Idiopathic Arthritis

The Etiology of Juvenile Idiopathic Arthritis

Gut microbiota-host interactions and juvenile idiopathic arthritis

The intestinal microbiome in spondyloarthritis

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