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TRIMELLITIC ANHYDRIDE-INDUCED EOSINOPHILLA IN A MOUSE MODEL OF OCCUPATIONAL ASTHMA
Citation:
Regal, J. F., M. E. Mohrman, AND D M. Sailstad. TRIMELLITIC ANHYDRIDE-INDUCED EOSINOPHILLA IN A MOUSE MODEL OF OCCUPATIONAL ASTHMA. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press, New York, NY, 175:234-242, (2001).
Impact/Purpose:
To determine if Trimellitic anhydride, a low molecular weight chemical known to cause occupational asthma, could elicit eosinophil infiltration into the lung of a sensitized mouse
Description:
Trimellitic anhydride (TMA) is a low molecular weight chemical known to cause occupational asthma. The present study was designed to determine if TMA could elicit eosinophil infiltration into the lung of a sensitized mouse similarly to previous studies with the protein allergen ovalbumin (OA). BALB/c mice were sensitized intradermally with TMA or OA followed by intratracheal instillation with TMA conjugated to mouse serum albumin (TMA-MSA) or OA. Non-sensitized mice received corn oil vehicle intradermally and MSA intratracheally. The allergic response was elicited 3 weeks later by intratracheal instillation of TMA-MSA, OA or control MSA. Cellular infiltration into bronchoalveolar lavage fluid (BAL) was determined 72 hours later. Eosinophil peroxidase (EPO) and myeloperoxidase (MPO) activity in the lung homogenates was used as an estimate of the numbers of eosinophils and neutrophils, respectively, in the lung tissue. In TMA-sensitized mice, TMA-MSA challenge significantly increased the numbers of eosinophils in the BAL and the EPO in lung indicating an increase in the number of eosinophils in the airway and tissue. In non-sensitized mice, TMA-MSA challenge also caused a small but significant increase in eosinophils in the BAL compared to the MSA control. Total IgE in both plasma and BAL was significantly higher in TMA-sensitized compared to non-sensitized mice. The eosinophil infiltration in TMA-sensitized mice was similar in magnitude to the response in OA-sensitized mice. These studies are the first to demonstrate TMA-induced eosinophilia in mouse lung and will provide the basis for comparing mechanisms and mediators responsible for the substantial eosinophilia induced by TMA and OA.
Key Words: trimellitic anhydride; mouse; occupational asthma; eosinophils; lung; pulmonary allergy.
