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AN EXTRACT OF STACHYBOTRYS CHARTARUM CAUSES ALLERGIC RESPONSE IN A BALB/C MOUSE MODEL
Citation:
Viana, M. E., N. H. HaykalCoates, S H. Gavett, MJK Selgrade, S J. Vesper, AND MDW Ward. AN EXTRACT OF STACHYBOTRYS CHARTARUM CAUSES ALLERGIC RESPONSE IN A BALB/C MOUSE MODEL. TOXICOLOGICAL SCIENCES (2002).
Description:
ABSTRACT
Environmental exposure to Stachybotrys chartarum has been associated with adverse health effects in humans. The goal of this study was to assess soluble components of this fungus for allergenic potential. Five isolates of S. chartarum were combined and extracted to form a crude antigen preparation (SCE-1). Female BALB/c mice were sensitized by involuntary aspiration of SCE-1 and subsequently re-exposed at 2, 3, and 4 weeks. To distinguish immune from non-specific inflammatory effects, mice were exposed to 3 doses of Hank's Balanced Salt Solution (HBSS) and a final dose of SCE-1; or to 4 doses of BSA as a negative control protein. Serum and bronchoalveolar lavage fluid (BALF) were collected before the fourth aspiration (day 0), and at days 1, 3, and 7 following the final exposure, and lungs were fixed for histopathological examination. SCE-1-exposed mice displayed increased BALF total protein on days 0, 1, and 3, and increased lactate dehydrogenase (LDH) at days 1 and 3 compared to HBSS controls. BALF total cell numbers were elevated on each day, and differential counts of BALF cells showed neutrophilia on day 1, marked eosinophilia on all days, and increased numbers of lymphocytes at days 1, 3, and 7. Serum and BALF total IgE levels were elevated at all days, and BALF IL-5 levels were greatly increased (7-fold) on day 1. Mice exposed to a single dose of SCE-1 exhibited inflammatory responses but not allergic responses, while BSA-treated mice showed neither inflammatory nor allergic responses. Histopathology confirmed the biochemical findings. The data indicate a transient non-specific inflammatory response followed a single or multiple exposure to SCE-1. Following multiple exposures, there was a more sustained immune-mediated eosinophilia and IgE response. We conclude that multiple respiratory exposures to SCE-1 cause responses typical of allergic airway disease in this mouse model, and that BSA can serve as a negative control protein when administered by this route.