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INDUCTION OF DEPRESSION BY EXPOSURE TO DAMP ...

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Komulainen, 2002; Huttunen et al., 2003). Exposure of this cell line to fungal spores of<br />

indoor-associated genera, such as Aspergillus, Penicillium, and Stachybotrys, induces the<br />

production of pro-inflammatory cytokines IL-1, IL-6, and TNF-α (Murtoniemi et al.,<br />

2003; Huttunen et al., 2003). Studies show that bacteria have an even higher<br />

inflammatory potential than fungi, with actinomycetes being the most reactive (Huttunen<br />

et al., 2003; Jussila and Komulainen, 2002; Jussila et al., 2002; Jussila J. et al., 2001;<br />

Hirvonen et al., 2005).<br />

Many in vivo experiments include either aspiration or instillation of fungal spores<br />

or extracts from the spores in either the trachea or nasal passages. In most studies, the<br />

bronchial alveolar lavage fluid (BALF) was analyzed either for immune cell presence or<br />

levels of pro-inflammatory cytokines. Studies did show an appreciable inflammatory<br />

effect on pulmonary tissue (Viana et al., 2002; Flemming et al., 2004; Chung et al., 2005;<br />

Chung et al., 2007).<br />

Going beyond animal models, several surveys have been completed that measured<br />

antibody levels in serum of healthy control individuals and those that were exposed to<br />

moldy environments. One such study compared the antibody levels of three cohorts: 500<br />

patients exposed to moldy indoor environments who had reported neurological and other<br />

symptoms, 500 healthy control subjects, and 500 random blood samples of patients<br />

whose blood had been sampled for reasons other than mold exposure (Vojdani et al.,<br />

2003B). Approximately sixty of the exposure buildings were verified by environmental<br />

engineers and found to have elevated levels of fungal growth. The patients lived in these<br />

environments for periods from two weeks to two years. Their findings indicated a<br />

significant difference in elevated IgG, IgM, and IgA antibodies to antigens from<br />

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