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Tryptophan-induced lung disease: an immunophenotypic, immunofluorescent, and electron microscopic study
H D Tazelaar1, J L Myers, J G Strickler
1Department of Pathology, Mayo Clinic, Rochester, Minnesota.
Summary
L-tryptophan (LT) linked eosinophilia-myalgia syndrome (EMS) can cause lung damage. T-cells, particularly CD8+ cytotoxic cells, were found to be key players in the lung inflammation associated with LT-induced EMS.
Area of Science:
- Immunology
- Pulmonary Medicine
- Toxicology
Background:
- Eosinophilia-myalgia syndrome (EMS) is a serious condition linked to L-tryptophan (LT) supplementation.
- Pulmonary complications affect up to 60% of EMS patients, presenting as chronic interstitial pneumonia and hypertensive pulmonary arteriopathy.
Purpose of the Study:
- To investigate the cellular and ultrastructural changes in lung biopsies from patients with L-tryptophan-induced EMS.
- To identify the immune cells involved in the pathogenesis of LT-induced lung injury.
Main Methods:
- Analysis of open lung biopsies using immunohistochemistry with lymphoid cell antibodies.
- Transmission electron microscopy to examine cellular ultrastructure.
- Direct immunofluorescence for immunoglobulins and complement.
Main Results:
- The interstitial and perivascular infiltrates were predominantly T-cells, with a significant presence of CD8+ cytotoxic/suppressor cells.
- Alveolar macrophages were abundant, with rare polyclonal B-cells observed.
- Ultrastructural analysis confirmed T-cell infiltration and inflammation within vessel walls, but no fibrointimal thickening.
Conclusions:
- T-cells, especially CD8+ cytotoxic/suppressor cells, are likely integral to the lung injury mechanism in L-tryptophan-induced EMS.
- The findings suggest a cell-mediated immune response contributes to the pulmonary pathology of LT-EMS.