THE EFFECT OF DIESEL EXHAUST PARTICLES (DEP) AND CARBON BLACK (CB) ON THIOL CHANGES IN PULMONARY OVALBUMIN ALLERGIC SENSITIZED BROWN NORWAY RATS

Brown Norway rats were exposed by intratracheal instillation of saline, carbon black (CB), or diesel exhaust particles (DEP) (5 mg/kg) on day 1, followed by exposure to ovalbumin (OVA, 90 mg/m 3) or saline for 30 minutes on days 1, 8, 15, and 29. Animals were sacrificed on day 30. The DEP, CB, or OV...

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Published inExperimental lung research Vol. 28; no. 5; pp. 333 - 349
Main Authors Al-Humadi, Nabil H., Siegel, Paul D., Lewis, Daniel M., Barger, Mark W., Ma, Jane Y. C., Weissman, David N., Ma, Joseph K. H.
Format Journal Article
LanguageEnglish
Published Philadelphia, PA Informa UK Ltd 2002
Taylor & Francis
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Summary:Brown Norway rats were exposed by intratracheal instillation of saline, carbon black (CB), or diesel exhaust particles (DEP) (5 mg/kg) on day 1, followed by exposure to ovalbumin (OVA, 90 mg/m 3) or saline for 30 minutes on days 1, 8, 15, and 29. Animals were sacrificed on day 30. The DEP, CB, or OVA exposure alone did not result in abnormal levels of inflammatory cells, lactate dehydrogenase (LDH), or total protein in the lavage fluid. In combined OVA-DEP or OVA-CB exposure, however, these markers were significantly increased. The adjuvant effect of CB and DEP on OVA sensitization was evidenced by the marked increases in serum OVA-specific IgG (5.6-fold) and IgE (3.5-4 fold) levels, and the increase in interleukin-4 (IL-4) mRNA levels in lung tissue. The OVA exposure markedly reduced glutathione (GSH) levels in both cell types. In combined DEP-OVA exposure, the level of GSH in lymphocytes was further decreased, indicating a possible interactive effect between DEP and OVA exposures. These results show that both DEP and CB augmented OVA-induced allergic sensitization, and that particle composition of DEP may not be a critical factor for the adjuvant effect. OVA exposure causes significant depletion of intracellular GSH in lymphocytes, which may play a key role in OVA-mediated immune responses.
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ISSN:0190-2148
1521-0499
DOI:10.1080/01902140290091976