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 a L-tryptophan contaminant.

Abstract

This study was designed to clarify the important association between eosinophilia-myalgia syndrome (EMS) and the L-tryptophan contaminant, "Peak E." To determine the functional activation of eosinophils induced by Peak E, eosinophil cationic protein (ECP) release was examined. Peak E augumented 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 bioactive 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.

• Authors: K A Yamaoka, N Miyasaka, G Inuo, I Saito, J P Kolb, K Fujita, S Kashiwazaki
• Journal: Journal of clinical immunology (J Clin Immunol) Vol. 14 Issue 1 Pg. 50-60 (Jan 1994) ISSN: 0271-9142 [Print] Netherlands
• PMID: 8132737 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Blood Proteins
• Eosinophil Granule Proteins
• Interleukin-5
• RNA, Messenger
• Receptors, Interleukin
• Receptors, Interleukin-5
• 1,1'-ethylidene bis(tryptophan)
• Tryptophan
• Ribonucleases

Topics

• B-Lymphocytes (immunology)
• Base Sequence
• Blood Proteins (biosynthesis)
• Electrophoresis, Agar Gel
• Eosinophil Granule Proteins
• Eosinophilia-Myalgia Syndrome (etiology)
• Eosinophils (immunology)
• Humans
• Interleukin-5 (biosynthesis)
• Lymphocyte Activation
• Molecular Sequence Data
• Polymerase Chain Reaction
• RNA, Messenger (metabolism)
• Receptors, Interleukin (metabolism)
• Receptors, Interleukin-5
• Ribonucleases
• Spleen (immunology)
• T-Lymphocytes (immunology)
• Tryptophan (adverse effects, analogs & derivatives, immunology)
• Tumor Cells, Cultured