The Determination of Draining Lymph Node Cell Cytokine mRNA Levels in BALB/c Mice Following Dermal Sodium Lauryl Sulfate, Dinitrofluorobenzene, and Toluene Diisocyanate Exposure
Differential modulation has been demonstrated in interleukin-4 (IL-4), IL-10, and interferon gamma (IFN-γ) mRNA and protein secretion patterns of cells isolated from the draining lymph nodes of mice following exposure to T cell and respiratory sensitizers. Using a multiprobe ribonuclease protection...
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Veröffentlicht in: | Toxicology and applied pharmacology 2001-03, Vol.171 (3), p.174-183 |
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Sprache: | eng |
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Zusammenfassung: | Differential modulation has been demonstrated in interleukin-4 (IL-4), IL-10, and interferon gamma (IFN-γ) mRNA and protein secretion patterns of cells isolated from the draining lymph nodes of mice following exposure to T cell and respiratory sensitizers. Using a multiprobe ribonuclease protection assay, the following investigation examined the mRNA expression patterns of multiple cytokines associated with respiratory sensitization for modulation following exposure to chemicals known primarily to induce irritation (sodium lauryl sulfate), respiratory sensitization (toluene diisocyanate), or T cell-mediated hypersensitivity (dinitrofluorobenzene) responses. On days 0 and +5 female BALB/c mice were exposed to either test article or vehicle on the shaven dorsal lumbar region; on days +10 through +12 the mice received test article on the dorsal aspect of each ear. On day +13 animals were euthanized, draining lymph nodes were excised, and mRNA was isolated immediately or following 24 or 48 h of culture in the presence or absence of concanavalin (Con) A. Differential expression of cytokine mRNA was most notable following 24 h incubation with Con A. Modulation of IL-4, -10, and IFN-γ following chemical exposure was consistent with previous studies. In addition, IL-9, -13, and -15 were significantly elevated only following toluene diisocyanate exposure. Further investigations of these cytokines may provide additional insight into the mechanisms of chemically induced respiratory sensitization and provide endpoints for the detection of a chemical's ability to elicit IgE-mediated hypersensitivity responses. |
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ISSN: | 0041-008X 1096-0333 |
DOI: | 10.1006/taap.2000.9123 |