The role of monocytes and<i>SLC11A1</i>polymorphisms in the pathogenesis of<i>Chlamydia</i>-induced reactive arthritis

Chen, Yi-Jing; Rn, Li; Lin, Chang-Shen; Yen, Jeng‐Hsien

doi:10.3109/03009742.2012.729608

Cited by 6 publications

(3 citation statements)

References 13 publications

(14 reference statements)

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“…The exact pathogenesis of the Th1/Th2 imbalance is not understood, but it is not unlikely that genetic factors are involved . Various cytokine gene polymorphisms have been reported and include polymorphisms in monocyte and solute carrier family 11 member A1 (SLC11A1), TNF‐α (‐238) and TNFR polymorphisms …”

Section: Pathogenetic Mechanismscontrasting

confidence: 63%

“…19 Various cytokine gene polymorphisms have been reported and include polymorphisms in monocyte and solute carrier family 11 member A1 (SLC11A1), TNF-a (-238) and TNFR polymorphisms. [74][75][76] Finally, Butrimiene et al have suggested that TNF-a production is higher in patients with chronic ReA and, therefore, the Th1 response in chronic ReA is more dominant than that in acute ReA. Interestingly, in this study no differences were reported in the type II response between the patients with chronic and acute ReA.…”

Section: Pathogenetic Mechanismscontrasting

confidence: 41%

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Reactive Arthritis

Stavropoulos

Soura

Κανελλέας

et al. 2014

Acad Dermatol Venereol

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Reactive arthritis (ReA) is an immune-mediated seronegative arthritis that belongs to the group of spondyloarthropathies and develops after a gastrointestinal or genitourinary system infection. The condition is considered to be characterized by a triad of symptoms (conjunctivitis, arthritis and urethritis) although a constellation of other manifestations may also be present. ReA is characterized by psoriasiform dermatological manifestations that may resemble those of pustular psoriasis and, similar to guttate psoriasis, is a post-infectious entity. Also, the articular manifestations of the disorder are similar to those of psoriatic arthritis and both conditions show a correlation with HLA-B27. These facts have led several authors to suggest that there is a connection between ReA and psoriasis, listing ReA among the disorders related to psoriasis. However, the pathogenetic mechanism behind the condition is complex and poorly understood. Bacterial antigenicity, the type of host response (i.e. Th1/Th2 imbalance) and various genetic factors (i.e. HLA-B27 etc.) play an important role in the development of the disorder. It is unknown whether all the aforementioned factors are part of a mechanism that could be similar to, or share basic aspects with known psoriasis pathogenesis mechanisms.

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Section: Pathogenetic Mechanismscontrasting

confidence: 63%

Section: Pathogenetic Mechanismscontrasting

confidence: 41%

Reactive Arthritis

Stavropoulos

Soura

Κανελλέας

et al. 2014

Acad Dermatol Venereol

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“…accordingly, in the last 10 years, several studies on the association of SLC11A1 variants and Ra in different populations have been published 10,[18][19][20][21] . In addition, a possible association between a SLC11A1 promoter polymorphism and Ra severity 22 , or risk for idiopathic arthritis or juvenile rheumatoid arthritis, has been reported 23,24 . However, in a recent meta-analysis performed by archer, et al 9 , only a single significant association was detected between SLC11A1 variants and Ra, namely the Int4 snP (469+14G/C or rs3731865), with an oR: 1.60 (95% CI: 1.20-2.13).…”

Section: Resultsmentioning

confidence: 99%

The Role of NRAMP1/SLC11A1 Gene Variant D543N (1730G/A) in the Genetic Susceptibility to Develop Rheumatoid Arthritis in the Mexican Mestizo population

Niño-Moreno

Turrubiartes-Martínez

Oceguera-Maldonado

et al. 2017

RIC

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Causality of Chlamydiae in Arthritis and Spondyloarthritis: a Plea for Increased Translational Research

Zeidler

Hudson

2016

Curr Rheumatol Rep

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Current molecular genetic understanding of the metabolically active persistent infection state of Chlamydia trachomatis and Chlamydia pneumoniae in the synovium in patients with arthritis and spondyloarthritis favors a causal relationship. Here, we examine how adequately the accepted criteria for that etiologic relationship are fulfilled, emphasizing the situation in which these microorganisms cannot be cultivated by standard or other means. We suggest that this unusual situation of causality by chlamydiae in rheumatic disease requires establishment of a consensus regarding microorganism-specific terminology as well as the development of new diagnostic and classification criteria. Recent studies demonstrate the value of molecular testing for diagnosis of reactive arthritis, undifferentiated spondyloarthritis, and undifferentiated arthritis caused by C. trachomatis and C. pneumoniae in clinical practice. Data regarding combination antibiotic therapy is consistent with the causative role of chlamydiae for these diseases. Observations of multiple intra-articular coinfections require more research to understand the implications and to respond to them.

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The role of monocytes andSLC11A1polymorphisms in the pathogenesis ofChlamydia-induced reactive arthritis

Abstract: The bactericidal activity of monocytes in patients with ReA is lower than that in healthy controls. The SLC11A1 274C/T and 823C/T polymorphisms may be associated with the decreased bactericidal activity of the monocytes.

Cited by 6 publications

References 13 publications

Reactive Arthritis

Reactive Arthritis

The Role of NRAMP1/SLC11A1 Gene Variant D543N (1730G/A) in the Genetic Susceptibility to Develop Rheumatoid Arthritis in the Mexican Mestizo population

Causality of Chlamydiae in Arthritis and Spondyloarthritis: a Plea for Increased Translational Research

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