Abstract
This study was designed to clarify the important association between eosinophilia-myalgia syndrome (EMS) and thel-tryptophan contaminant, “Peak E.” To determine the functional activation of eosinophils induced by Peak E, eosinophil cationic protein (ECP) release was examined. Peak E augmented the release of ECP from peripheral blood normodense eosinophils by degranulation. Proliferative analysis using the human eosinophilic leukemia cell line EoL-3 showed prominent cellular replication in the presence of Peak E. Moreover, Peak E upregulated interleukin 5 (IL-5) receptor levels on normodense eosinophils. Of particular interest, Peak E-stimulated human splenic T cells produced bipactive and immunoreactive IL-5. Marked induction of IL-5 mRNA in Peak E-stimulated T cells was also shown by reverse-transcriptase polymerase chain reaction (RT-PCR). In contrast,l-tryptophan without the contaminant showed none of these effects. Thus, these data suggest that Peak E might be involved in the pathogenesis of EMS through bimodal mechanism including IL-5 generation by T cells and potentiation of eosinophil functional activation.
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Yamaoka, K.A., Miyasaka, N., Inuo, G. et al. 1,1′-Ethylidenebis(tryptophan) (peak E) induces functional activation of human eosinophils and interleukin 5 production from T lymphocytes: Association of eosinophilia-myalgia syndrome with al-tryptophan contaminant. J Clin Immunol 14, 50–60 (1994). https://doi.org/10.1007/BF01541175
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DOI: https://doi.org/10.1007/BF01541175