Section of Rheumatology, Medicine Department, LSU Health Sciences Center, New Orleans, LA, USA
Correspondence to: L. R. Espinoza, 1542 Tulane Avenue, New Orleans, LA 70112, USA. E-mail: rcucha{at}hotmail.com or rcucha{at}lsuhsc.edu
SIR, We read with great interest the study by Bas et al. [1] in which they analysed synovial fluid (SF) cytokine levels in reactive arthritis (ReA), rheumatoid arthritis (RA) and osteoarthritis, and correlate them with the HLA-B27 haplotype in a subset of ReA patients positive for Chlamydia trachomatis. The results did not reveal significant differences in cytokine levels and ratios among the groups, although lower levels of interferon (IFN-
) in SF were found in the HLA-B27-positive ReA patients than in the negative ones.
The data presented are striking, but they merit comment. First, the Quantikine ELISA kits used are not validated for use with SF. Therefore, it is fair to ask why these kits were used to analyse the SF.
Secondly, the lower levels of SF interleukin (IL) 10 in ReA than in RA are at variance with other reports. In addition, how do the authors explain the higher ratios of IFN- to IL-10 among the ReA patients? Animal models of Chlamydia infection have shown that the clearance of the organism is affected by the balance between IFN-
and IL-10, and IL-10 gene knockout mice clear Chlamydia infection more rapidly than normal [24].
We also wonder why IL-4 and IL-17 were not analysed. Considering that the immune response to Chlamydia requires a Th1 response, it would have been of interest to demonstrate the adequacy or inadequacy of this response by determining the presence of IL-4. In addition, IL-17 is relevant to joint destruction, and its presence in the joints of ReA patients is of obvious interest and importance [4].
The authors have declared no conflicts of interest.
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