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TRIMELLITIC ANHYDRIDE-INDUCED EOSINOPHILIA IN A MURINE MODEL OF OCCUPATIONAL ASTHMA
Citation:
Regal, J. F., M. E. Mohrman, E H. Boykin, AND D M. Sailstad. TRIMELLITIC ANHYDRIDE-INDUCED EOSINOPHILIA IN A MURINE MODEL OF OCCUPATIONAL ASTHMA. Presented at SOT, San Francisco, CA, March 25-29, 2001.
Description:
TRIMELLITIC ANHYDRIDE-INDUCED EOSINOPHILIA IN A MURINE MODEL OF OCCUPATIONAL ASTHMA. J F Regal, ME Mohrman, E Boykin and D Sailstad. Dept. of Pharmacology, University of Minnesota, Duluth, MN, USA and NHEERL, ORD, US EPA, RTP, NC, USA.
Trimellitic anhydride (TMA) is a small molecular weight chemical known to cause occupational asthma. To determine if TMA elicits cell infiltration into the lung similar to eosinophilia described for the protein allergen ovalbumin (OA), BALB/c mice were sensitized as follows: days 1 and 3 intradermally with either 3% TMA, 0.3% OA, or corn oil vehicle (non-sensitized); day 12 intratracheally with either 30 g of TMA conjugated to mouse serum albumin (TMA-MSA), OA, or MSA as control. To elicit the response, mice were challenged intratracheally on days 19, 22, and 23 with either 30 g TMA-MSA, OA or control MSA. Cell infiltration in bronchoalveolar lavage (BAL) was assessed 72 hr later. In TMA-sensitized mice, challenge with TMA-MSA resulted in a significant increase in the BAL eosinophils to 24.7+5.2% of total white blood cells compared to MSA challenged mice with 1.3+0.3% eosinophils. No differences were detected in macrophages or neutrophils in the BAL. Furthermore, TMA-MSA challenge also significantly increased eosinophil peroxidase in lung homogenates indicating an increase in eosinophils in the tissue. In non-sensitized mice, TMA-MSA challenge caused a small but significant increase in eosinophils in BAL (1.5+0.4%) compared to the MSA control (0.5+0.1%). Total IgE in both plasma and BAL was significantly higher in TMA-sensitized compared to non-sensitized mice. The eosinophilia in TMA-sensitized mice was similar to the response seen in OA-sensitized and challenged mice. These studies provide the basis for examination of mechanisms and mediators responsible for the substantial TMA-induced eosinophilia. This model also provides a baseline response of eosinophilia to compare alternate methods of sensitization and elicitation in developing screening methods for small molecular weight respiratory allergens. (Supported in part by NIH ES 07406. This abstract does not reflect EPA policy).