Infectious Aspects and the Etiopathogenesis of Rheumatoid Arthritis

Meron, Michal Kasher; Amital, Howard; Shepshelovich, Daniel; Barzilai, Ori; Ram, Maya; Anaya, Juan Manuel; Gerli, Roberto; Bizzaro, Nicola; Shoenfeld, Yehuda

doi:10.1007/s12016-009-8158-6

Cited by 49 publications

(23 citation statements)

References 25 publications

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“…Clinical and animal model studies have suggested that infections by many micro-organisms, such as Porphyromonas gingivalis (Bartold et al , 2010; Hitchon et al , 2010), Proteus mirabilis (Arabski et al , 2012), Epstein–Barr virus (Mourgues et al , 2016) and mycoplasma contribute to the aetiopathogenesis of RA (Durigon et al , 1993). Higher rates of serological evidence of infections with Epstein–Barr virus and cytomegalovirus were detected in RA patients than in population controls (Magnusson et al , 2010; Meron et al , 2010). …”

Section: Introductionmentioning

confidence: 91%

Frequency and significance of parvovirus B19 infection in patients with rheumatoid arthritis

Naciute

Mieliauskaitė

Rugienė

et al. 2016

Journal of General Virology

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The present study aims to clarify the possible involvement of parvovirus B19 (B19V) infection in rheumatoid arthritis (RA) pathogenesis by investigating the presence of B19V infection markers (genomic sequences and virus-specific antibodies) in association with the level of cytokines and RA clinical activity and aggressiveness. A total of 118 RA patients and 49 age- and sex-matched healthy volunteers were enrolled in the study. Nested PCR was used to detect B19V sequences in whole blood and cell-free plasma DNA, ELISA to detect virus-specific antibodies and cytokine levels in plasma and recomLine dot blot assay for antibodies to separate B19V antigens. The detection frequency of B19V DNA was higher in patients with RA (25.4 %) in comparison with healthy persons (18.4 %). B19V DNA in cell-free plasma (B19+p) was detected significantly often in RA patients in comparison with healthy controls (13.6 vs 2 %; P=0.0002). RA B19+p patients had higher disease activity and aggressiveness, decreased haemoglobin and increased erythrocyte sedimentation rates. IL-6 plasma levels were significantly higher in RA patients than in controls. Within the RA patients’ group the IL-6 level was significantly increased in B19+p patients with disease activity scores of DAS28>5.2, high C-reactive protein and low haemoglobin. Contrary to the healthy controls, the majority of RA B19+p patients did not have antibodies to VP-1S (VP1u) and VP-N (N-terminal half of structural proteins VP1 and VP2), which correspond to the epitopes of neutralizing antibodies. These results indicate that B19V infection at least in some patients is involved in RA pathogenesis.

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Section: Introductionmentioning

confidence: 91%

Frequency and significance of parvovirus B19 infection in patients with rheumatoid arthritis

Naciute

Mieliauskaitė

Rugienė

et al. 2016

Journal of General Virology

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“…Yamanishi et al [22] found increased IgM rheumatoid factor in B cells chronically stimulated with H. pylori urease. However, several studies demonstrated that there is a lower prevalence of H. pylori in RA patients, and other studies found the prevalence of H. pylori to be similar to that of the healthy controls [27,34,35] . After H. pylori eradication, no change in RA symptoms was reported by several studies [36][37][38] , although improvement was noted in others [39,40] .…”

Section: Rheumatoid Arthritismentioning

confidence: 97%

Helicobacter pyloriand autoimmune disease: Cause or bystander

Smyk¹,

Κουτσουμπασ²,

Mytilinaiou³

et al. 2014

WJG

148

108

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Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research.

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“…Sera from RA patients contain high titres of Epstein-Barr virus (EBV) antigens and of antibodies to latent and replicative EBV antigens. In addition, EBV RNA has been identified in B cells in synovial tissue from RA patients [35]. Despite these findings, the evidence that microorganisms are involved in the development of RA remains inconclusive.…”

Section: Infectionsmentioning

confidence: 99%