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Biomedical subjects

Denise M Sailstad

Publications and source records attributed to Denise M Sailstad.

3 recordsLinked to original sources
PubMed2004

Ultraviolet radiation downregulates allergy in BALB/c mice.

The immunosuppressive effects of exposure to ultraviolet radiation (UVR) are well known and the underlying mechanisms extensively studied. The suppression of Th1 appears to account for UVR suppression of contact hypersensitivity and delayed-type hypersensitivity responses and increased susceptibility to certain infections and tumor development. The underlying mechanisms suggest Th2-mediated responses associated with immediate-type hypersensitivity and allergic lung disease should be unchanged or possibly enhanced by UVR. The hypothesis that UVR exposure enhances allergic lung disease in BALB/c mice was tested. Effects of UVR on sensitization and elicitation of respiratory hypersensitivity were assessed using a fungal extract, Metarhizium anisopliae (MACA), as the allergen. BALB/c mice were sham or UVR (8 KJ/m(2)) exposed 3d before involuntary aspiration (IA) of MACA or vehicle. The mice received UVR exposures before the first and second of three IAs in the sensitization protocol and 3 d before the fourth IA in the elicitation protocol. Serum and bronchoalveolar lavage fluid (BALF) were harvested before (d 21, sensitization/d 24, elicitation) and at 1 (d 22/d 28), 3 (d 24/d 29), and 7 (d 28/d 35) d following the last IA. UVR exposure prior to sensitization suppressed two hallmarks of allergic disease, immune-mediated inflammation (eosinophil influx) and total immunoglobulin (Ig)E compared to the sham-UVR controls. There were no differences attributable to UVR exposure in previously sensitized mice. These data suggest that UVR exposure prior to sensitization suppresses allergic responses but has no effect on the elicitation of allergic responses in previously sensitized individuals. Consequently, there is no evidence that exposure to UVR enhances the induction or expression of allergic lung disease.

Animals↗
PubMed2003

A murine model for low molecular weight chemicals: differentiation of respiratory sensitizers (TMA) from contact sensitizers (DNFB).

Exposure to low molecular weight (LMW) chemicals contributes to both dermal and respiratory sensitization and is an important occupational health problem. Our goal was to establish an in vivo murine model for hazard identification of LMW chemicals that have the potential to induce respiratory hypersensitivity (RH). We used a dermal sensitization protocol followed by a respiratory challenge with the evaluation of endpoints typically associated with RH in human disease. Trimellitic anhydride (TMA) was used as a prototype respiratory sensitizer and was compared to the dermal sensitizer; 2,4-dinitrofluorobenzene (DNFB), along with vehicle controls. BALB/c mice were dermally sensitized using two exposure protocols. Mice in both protocols were dermally exposed on experimental days; D-18 and D-17 (abdomen), and D-13 (ear). On D 0 mice received an intratracheal (IT) challenge. The mice in Protocol 2 were abdominally exposed twice with the addition of exposures on D-25 and D-24. Results indicate that mice required the additional dermal sensitization and the IT challenge (Protocol 2) to significantly elevate total IgE in serum and bronchoalveolar lavage fluid (BALF). Additional responses suggestive of RH were seen following Protocol 2, including increases in BALF cell numbers and neutrophils post IT with TMA (but not DNFB). These data suggest that the dermal sensitization and IT challenge followed by evaluation of serum antibodies and lung parameters are a reasonable and logistically feasible approach towards the development of a model for RH responses to LMW chemicals.

Administration, Inhalation↗