This page lists medical journal articles discussing how inflammation and oxidative stress may be related to exposure to moldy buildings.
The Health Effects of Moldy Buildings page of the Paradigm Change site provides further information on this topic.
Bossou YM, Serssar Y, Allou A, Vitry S, Momas I, Seta N, Menotti J, Achard S. Impact of Mycotoxins Secreted by Aspergillus Molds on the Inflammatory Response of Human Corneal Epitheal Cells. Toxins (Basel). 2017 Jun 22;9(7). PMID: 28640227
The present study investigates the effects of aflatoxin B₁ (AFB₁) and gliotoxin, two mycotoxins secreted by Aspergillus molds, on the biological activity of the human corneal epithelial (HCE) cells. Gliotoxin appeared more cytotoxic than AFB₁ but, at the same time, led to a lower increase of the inflammatory response reflecting its immunosuppressive properties. Real-time cell impedance measurement showed a distinct profile of cytotoxicity for both mycotoxins. Low, but persistent inflammation, caused by environmental factors, such as fungal toxins, leads to irritation and sensitization, and could be responsible for allergic manifestations which, in turn, could lead to mucosal hyper-reactivity.
Rosenblum Lichtenstein JH, Hsu YH, Gavin IM, Donaghey TC, Molina RM, Thompson KJ, Chi CL, Gillis BS, Brain JD. Environmental mold and mycotoxin exposures elicit specific cytokine and chemokine responses. PLoS One. 2015 May 26;10(5):e0126926. PMID: 26010737
We sought to use isolated peripheral blood mononuclear cells (PBMCs) to understand changes in cytokine and chemokine levels in response to mold and mycotoxin exposures and to link these levels with respiratory symptoms in humans. Peripheral blood mononuclear cells (PBMCs) were isolated from blood from 33 patients with a history of mold exposures and from 17 controls. These findings demonstrate that chronic mold exposures induced changes in inflammatory and immune system responses to specific mold and mycotoxin challenges. These responses can differentiate mold-exposed patients from unexposed controls. This strategy may be a powerful approach to document immune system responsiveness to molds and other inflammation-inducing environmental agents.
Guilford FT, Hope J. Deficient glutathione in the pathophysiology of mycotoxin-related illness. Toxins (Basel). 2014 Feb 10;6(2):608-23. PMID: 24517907
Evidence for the role of oxidative stress in the pathophysiology of mycotoxin-related illness is increasing. The glutathione antioxidant and detoxification systems play a major role in the antioxidant function of cells. Exposure to mycotoxins in humans requires the production of glutathione on an “as needed” basis. Research suggests that mycotoxins can decrease the formation of glutathione due to decreased gene expression of the enzymes needed to form glutathione. Mycotoxin-related compromise of glutathione production can result in an excess of oxidative stress that leads to tissue damage and systemic illness. The review discusses the mechanisms by which mycotoxin-related deficiency of glutathione may lead to both acute and chronic illnesses.
Lappalainen MH, Hyvärinen A, Hirvonen MR, Rintala H, Roivainen J, Renz H, Pfefferle PI, Nevalainen A, Roponen M, Pekkanen J. High indoor microbial levels are associated with reduced Th1 cytokine secretion capacity in infancy. Int Arch Allergy Immunol. 2012;159(2):194-203. PMID: 22678428
High indoor microbial exposures may affect immune development in early life by reducing T helper type 1 cytokine secretion capacity. A high total level of the studied Gram-positive bacteria in general or Mycobacterium spp. in house dust was associated with decreased SEB-stimulated IFN-γ production, especially at the age of 1 year. The total level of indoor fungi analyzed (Penicillium spp., Aspergillus spp. and Paecilomyces variotii group, Trichoderma viride/atroviride/koningii,Wallemia sebi) was also inversely associated with IFN-γ production at the age of 1 year, but this association did not remain significant after adjustment for potential confounders. The observed hyporesponsiveness may reflect the adaptation of the immune system to environmental antigens. In future, more attention should be paid especially to the immunomodulatory role of exposures to Gram-positive bacteria.
Allermann L, Wilkins CK, Madsen AM. Inflammatory potency of dust from the indoor environment and correlation to content of NAGase and fungi. Toxicol In Vitro. 2006 Dec;20(8):1522-31. PMID: 16930940
The aim of this study was to analyse the contribution of microbial factors to the inflammatory potency of dust (PD). Floor dust was sampled three times from 12 rooms in two schools. The potency of floor dust was measured as interleukin-8 secretion from the lung epithelial cell line A549 after exposure to dust. Microbiological activity especially from fungi may contribute to the inflammatory potency of floor dust. Carpet flooring may act as a “sink” for microorganisms resulting in a higher inflammatory potency of floor dust, which may reflect building-related symptoms in occupants.
Hirvonen MR, Huttunen K, Roponen M. Bacterial strains from moldy buildings are highly potent inducers of inflammatory and cytotoxic effects. Indoor Air. 2005;15 Suppl 9:65-70. PMID: 15910531
We aimed to identify inflammatory and cytotoxic potential of individual indoor air bacterial and fungal strains, as well as extracts of indoor air filter samples containing bacteria and fungi. Mouse RAW264.7 macrophages were exposed in vitro to four bacterial strains; Streptomyces californicus, Mycobacterium terrae, Bacillus cereus and Pseudomonas fluorescens, and three fungal strains; Penicillium spinulosum, Aspergillus versicolor and Stachybotrys chartarum. Furthermore, RAW264.7 macrophages were exposed to indoor air filter sample extracts representing ‘low’ (n = 21) and ‘high’ (n = 20) exposure to viable fungi or bacteria. The results show that the bacterial strains induce more profound production of NO, TNF-alpha and IL-6 than the studied fungal strains. They also decrease the viability of mouse macrophages. Similarly, the indoor air filter samples with high concentration of bacteria induced a statistically significant increase in TNF-alpha and IL-6 production as well as a decrease in cell viability.
Links on this page are in orange (no underlining).