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EFFECT OF DIESEL EXHAUST EXPOSURE ON MUCOSAL SENSITIZATION TO OVALBUMIN ANTIGEN.
Citation:
STEVENS, T., M. J. DANIELS, E. BOYKIN, W. P. LINAK, AND M.(IAN) I. GILMOUR. EFFECT OF DIESEL EXHAUST EXPOSURE ON MUCOSAL SENSITIZATION TO OVALBUMIN ANTIGEN. . Presented at 45th Annual Society of Toxicology Meeting 2006, San Diego, CA, March 05 - 09, 2006.
Description:
Several studies in humans and animals have shown that diesel exhaust (DE) can act as an immunological adjuvant to increase the severity of Type I hypersensitivity immune responses. The mechanism by which DE causes these effects is unknown but thought to be associated with lung injury and inflammation. This study utilized a freshly generated inhalation exposure along with mucosal sensitization and challenge with ovalbumin antigen. Balb/C mice were exposed to air, 0.5, or 2 mg/m3 for 4 hours a day for 5 days. After the diesel exposure on the first three days, mice were anesthetized and exposed intranasally to 100 ?g ovalbumin in 20 ?l of PBS. On Days 18 and 28, mice were challenged intranasally with 100 ?g OVA in 20 ?l PBS, and euthanized 24, 48, and 96 hours after the last challenge. Immune and inflammatory markers were then assessed in serum, lungs and lymph nodes. The results showed no significant changes in biochemical markers of injury and edema in lung lavage fluid at any time. Pulmonary cell differential counts showed an increase in neutrophils at the high dose as early as 24 hrs after the last challenge. Both low and high diesel groups had increased neutrophils at 48 which subsided by 96 hrs. Eosinophils showed an increasing trend in both low and high diesel groups at the 48 and 96 h time points. Lymphocytes were also increased in both diesel groups at the 48 and 96 time points. Ova specific IgE increased above control (air-exposed animals) levels at the 48 h time point in the high dose diesel. Collectively the results demonstrate that diesel exhaust generated in this system causes mild adjuvant effects in a mouse model employing local (mucosal) sensitization. Further analysis of gene expression in lung and lymph nodes at the early timepoints are underway to identify signaling pathways responsible for this effect. (This abstract does not reflect EPA policy).