Abstract

Exposure to mold in water-damaged buildings can have severe adverse effects on human health. Despite evidence that mold exposure causes increased anxiety, depression, chronic fatigue, pain, and cognitive problems, no animal research has been published examining how mold exposure causes these problems. We examined the effects of exposing mice to spores of Stachybotrys chartarum, probably the most studied of the damp-building molds. Mice were exposed to either intact Stachybotrys spores, containing a variety of potent toxins and proteinases, to spores extracted twice with alcohol to remove spore contents, or to saline vehicle. Although intact spores cause greater immune activation in the lungs, in all cases, extracted spores caused the same degree of short- and long-term memory loss as intact spores. Memory deficits were specific to hippocampal memory. Long-term memory deficits were correlated with the numbers of amoeboid microglia in the hippocampus in mice exposed to intact mold spores. This correlation was not found in mice treated with extracted spores, although these mice had the same memory deficits. Mold exposure also caused significant changes in IL-1beta immunoreactivity in the hippocampus. Since the innate immune system has multiple receptors that recognize skeletal elements of mold spores, our data suggest that respiratory exposure to any mold, not just the particularly toxic ones like Stachybotrys, may be capable of causing brain inflammation and memory loss.

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