1,1'-ETHYLIDENEBIS(TRYPTOPHAN) (PEAK-E) INDUCES FUNCTIONAL ACTIVATIONOF HUMAN EOSINOPHILS AND INTERLEUKIN-5 PRODUCTION FROM T-LYMPHOCYTES - ASSOCIATION OF EOSINOPHILIA-MYALGIA-SYNDROME WITH A L-TRYPTOPHAN CONTAMINANT

This study was designed to clarify the important association between e osinophilia-myalgia syndrome (EMS) and the L-tryptophan contaminant, ' 'Peak E.'' To determine the functional activation of eosinophils induc ed by Peak E, eosinophil cationic protein (ECP) release was examined. Peak E augmented the release of ECP from peripheral blood normodense e osinophils by degranulation. Proliferative analysis using the human eo sinophilic leukemia cell line EoL-3 showed prominent cellular replicat ion in the presence of Peak E. Moreover, Peak E upregulated interleuki n 5 (IL-5) receptor levels on normodense eosinophils. Of particular in terest, Peak E-stimulated human splenic T cells produced bioactive and immunoreactive IL-5. Marked induction of IL-5 mRNA in Peak E-stimulat ed T cells was also shown by reverse transcriptase polymerase chain re action (RT-PCR). In contrast, L-tryptophan without the contaminant sho wed none of these effects. Thus, these data suggest that Peak E might be involved in the pathogenesis of EMS through bimodal mechanism inclu ding IL-5 generation by T cells and potentiation of eosinophil functio nal activation.