title: Effect of L-tryptophan supplementation on eosinophils and eotaxin in guinea pigs.
abstract: Eosinophilia Myalgia Syndrome is a hypereosinophilic disorder that appears to result from the ingestion of the dietary supplement L-tryptophan by susceptible individuals. It is unclear if this disease results from tryptophan, contaminants found in tryptophan, individual predisposition (such as immune status and allergies), or some combination of effects. To evaluate effects of L-tryptophan on eosinophil migration, guinea pigs were compared with or without supplemental tryptophan (0.4 g/kg/day), with or without immune sensitization, and with or without immune challenge. Eosinophil counts were obtained from bone marrow, blood, lung, and bronchial alveolar lavage fluid (BAL). Lung cells were obtained to measure eotaxin concentrations in supernates and lysates with or without antigen and calcium ionophore challenge using direct ELISA. Skin biopsies were taken from both non-injected and antigen injection sites. The tryptophan supplemented, antigen-sensitized/antigen-challenged guinea pigs showed a significant decrease in blood eosinophils, compared to control (cellulose) supplemented antigen-sensitized/antigen-challenged guinea pigs [(0.086 +/- 0.023) x 10(6) vs (0.147 +/- 0.021) x 10(6) eosinophils/ml recovered, respectively] with a significant increase in BAL eosinophils [(0.052 +/- 0.008) x 10(6) vs (0.033 +/- 0.005) x 10(6) eosinophils/ml recovered, respectively]. Unchallenged lung cell lysates from tryptophan-supplemented guinea pigs contained significantly less eotaxin compared to cellulose-supplemented guinea pigs regardless of whether they were sensitized (0.006 +/- 0.002 vs 0.027 +/- 0.008 ng/10(6) cells, respectively). No differences were observed in skin biopsies between cellulose and tryptophan groups. These results suggest that L-tryptophan-supplemented guinea pigs have altered eotaxin regulation, a potential mechanism by which human overconsumption of tryptophan dietary supplements could lead to hypereosinophilic disorders in susceptible individuals.
authors.affiliation: Department of Medicine, University of Wisconsin-Madison, 53706, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Stahl
authors.forename: E B
authors.initials: EB
authors.lastname: Cook
authors.forename: M A
authors.initials: MA
authors.lastname: Pariza
authors.forename: M E
authors.initials: ME
authors.lastname: Cook
authors.forename: F M
authors.initials: FM
authors.lastname: Graziano
mesh_terms: D000818:Animals; D001835:Body Weight; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects*; D006168:Guinea Pigs; D007958:Leukocyte Count; D012867:Skin / Q000378:metabolism / Q000473:pathology; D014364:Tryptophan / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D014364:Tryptophan