Abstract
We read with great interest the contribution by Bazso et al. [1]. They reported the case of a 12-year-old girl with juvenile idiopathic arthritis (JIA) who developed systemic lupus erythematosus (SLE) after 10 years and speculated a few hypotheses of “shared autoimmunity,” the complete dysregulation of the immune system, and the side eVect of the anti-TNF therapy. However, we would like to suggest a diVerent and possible pathomechanism of the overlapping JIA and SLE case. The patient presented Escherichia coli (E. coli) septicemia at the age of 22 and subsequently developed clinical, immunological, and pathological manifestations fulWlling the diagnostic criteria of SLE within the following 8 weeks. SigniWcantly, Uthman et al. [2] also reported a case of SLE following E. coli sepsis in a 72-year-old woman, postulating three plausible pathomechanisms. Firstly, Robertson and Pisetsky [3] reported that Wve of the eight patients with E. coli bacteremia demonstrated increased levels of antibodies to single-stranded (ss) DNA from E. coli. Secondly, Gilkeson et al. [4] showed that normal mice immunized with ssDNA derived from E. coli developed an immune-mediated proliferative glomerulonephritis secondary to renal deposition of anti-DNA antibodies as in SLE. Thirdly, E. coli is known to produce heat shock protein (HSP), and Schultz et al. [5] suggested a role of HSP in the pathogenesis of rheumatic diseases like SLE. The host initially reacts to microbial infections with an enhanced cellular and humoral response to the microbial HSP, and cross-reactivity may occur with the HSP of the stressed host because of structural similarities to the microbial HSP [5]. Therefore, there is a possibility that E. coli septicemia might play a critical role as an inducer in the development of SLE in the Bazso et al.’s patient. However, further studies are necessary to elucidate the exact relationship and molecular pathogenic pathway between the JIA and SLE overlap in the future.
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