INDUCTION OF DEPRESSION BY EXPOSURE TO DAMP ...

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inflammatory reaction in allergic mouse models exposed to fungal spores than non- allergic exposed to fungal spore models and control allergic models. A Th1 inflammatory reaction is a delayed reaction, and as discussed earlier, may result in a more chronic inflammatory condition. This raises the question as to whether non-atopic individuals are more prone to the depression-inducing chronic inflammation from exposure to damp spaces than atopic individuals. Beyond allergic tendencies, people with underlying conditions that result in chronic inflammation may be predisposed inflammatory reactions from exposure to damp buildings and the resulting neurological insult. As an example of such an effect, Teeling and Perry discuss that people with inflammatory diseases have more depression with IFN-α treatment (Teeling and Perry, 2009). Teeling goes on to discuss that astrocytes (which includes microglia) proliferate due to inflammation, which go on to release additional inflammatory cytokines. Excessive astrocyte numbers are seen in several CNS-related diseases, such as multiple sclerosis, Alzheimer’s disease, and stroke. Thus, genetic propensity for poor regulation of astrocyte proliferation due to underlying chronic inflammation may be a risk factor. Shoemaker, Hudnell and colleagues have produced several publications reporting evidence for a genetic component underlining exaggerated and chronic inflammatory reactions associated with damp buildings. Their work began with documenting inflammatory reactions in susceptible people caused by the estuarine dinoflagellate, Pfiesteria piscidia (Hudnell, 2005; Shoemaker and Hudnell, 2001). The susceptible people experienced multiple symptoms and increased levels of inflammatory markers with exposure to P. piscidia blooms in estuaries. Because of their work, a disease 24
described as possible estuary-associated syndrome (PEAS) was recognized by the United States Centers for Disease Control. Continuing their work on inflammatory diseases from biological exposures, this group then found the same increase in immune markers and multi-system symptoms in some individuals exposed to damp buildings (Shoemaker and House, 2006). Abnormal inflammatory levels and symptoms were alleviated in both PEAS and damp building exposure through the use of cholestyramine and immune modulating drugs. Cholestyramine is a chelating agent that is typically used to lower cholesterol, although it can also remove chemical and biological agents from the intestines. One hypothesis is that inflammagenic agents from damp buildings are not eliminated from the body in genetically susceptible individuals. Hypothetically, the agents would eventually be transported into the intestines by the liver and then migrate through the intestinal wall back into the body. Cholestyramine in the intestines would act as a chelating agent, binding and removing the agents. Genetic data compiled from individuals that reportedly have been successfully treated using the cholestyramine therapy suggests that certain human leukocyte antigen (HLA) genes may be responsible for the susceptibility. Specific alleles associated with susceptibility included certain Class II HLA-DR and –DQ loci (Hudnell, 2005). This genetic data may partly answer why only a minority of the population appears to be significantly impacted by exposures to damp buildings. Beyond HLA genotypes, other genetic factors are also likely involved. Dysregulation of the body’s systems resulting in depression and immunological irregularities due to genetic polymorphisms is well documented. Similar polymorphisms 25
Page 1: UNIVERSITY OF WISCONSIN-LA CROSSE G
Page 4 and 5: TABLE OF CONTENTS Introduction ....
Page 6 and 7: generalized and chronic inflammatio
Page 8 and 9: As support for the monoamine hypoth
Page 10 and 11: psychological/physiological syndrom
Page 12 and 13: The similarities between symptoms o
Page 14 and 15: noradrenaline availability. Noradre
Page 16 and 17: While neurogenesis is most active i
Page 18 and 19: al., 2008). However, increasing NMD
Page 20 and 21: A polymorphism in a chaperone prote
Page 22 and 23: of prostaglandins, thromboxanes, an
Page 24 and 25: the result of exposure to chemicals
Page 26 and 27: 202 unexposed individuals, the pati
Page 30 and 31: may be a factor in chronic inflamma
Page 32 and 33: to 10-100 times greater than that f
Page 34 and 35: While some studies have provided ad
Page 36 and 37: few exceptions, many of the genera
Page 38 and 39: Penicillium notatum, Aspergillus ni
Page 40 and 41: Motile bacteria Flagellin TLR-5 Gra
Page 42 and 43: al., 2007). One study exposed mice
Page 44 and 45: complement present in the plasma as
Page 46 and 47: Fungal and Bacterial Hemolysins and
Page 48 and 49: Donohue and colleagues found that 1
Page 50 and 51: mycotoxins in relation to health ha
Page 52 and 53: References Afrah, A., Gustafsson, H
Page 54 and 55: Cameron, H., McEwen, B., & Gould, E
Page 56 and 57: Fang, L., Clausen, G., & Fanger, P.
Page 58 and 59: A: kinetics and potentiation by bac
Page 60 and 61: Miotto, D., hollenberg, M., Bunnett
Page 62 and 63: Park, J., & Ikeda, K. (2006) Variat
Page 64 and 65: Shoemaker, R., & House, D. (2006) S
Page 66: Wichers, M., Koek, G., Robaeys, G.,

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