This page lists medical journal articles discussing immune system issues associated with Stachybotrys exposures.
The Health Effects of Stachybotrys Chartarum page of the Paradigm Change site provides further information on the effects of this toxic mold.
Kim JH, Harvey LA, Evans AL, Byfield GE, Betancourt DA, Dean TR. Biological responses of Raw 264.7 macrophage exposed to two strains of Stachybotrys chartarum spores grown on four different wallboard types. Inhal Toxicol. 2016 Jun;28(7):303-12. PMID: 27097835
The focus of this research was to determine the effects of Stachybotrys chartarum (strains Houston and 51-11) grown under different conditions on a macrophage cell line (Raw 264.7) using endpoints, including cytotoxicity, and those associated with immunity specifically inflammation and MHC class II expression. The fungi were grown on four different gypsum products, and macrophages were exposed to whole spores of both strains and fragmented spores of strain 51-11. Whole spores of the Houston strain elicited no cytotoxicity with some level of inflammation, while exposure to whole spores of 51-11 caused variable responses depending on the wallboard type supporting the fungal growth. High concentrations of fragmented 51-11 spores primarily resulted in the apoptosis of macrophage with no inflammation. Collectively, the data demonstrated that all of the wallboard types supported growth of fungi with the ability to elicit harmful biological responses with the potential to negatively impact human health.
Rosenblum Lichtenstein JH, Molina RM, Donaghey TC, Hsu YH, Mathews JA, Kasahara DI, Park JA, Bordini A, Godleski JJ, Gillis BS, Brain JD. Repeated Mouse Lung Exposures to Stachybotrys chartarum Shift Immune Response from Type 1 to Type 2. Am J Respir Cell Mol Biol. 2016 Oct;55(4):521-531. PMID: 27148627
After a single or multiple intratracheal instillations of Stachybotrys chartarum (S. chartarum or black mold) spores in BALB/c mice, researchers found marked differences in BAL cell counts, especially large increases in lymphocytes and eosinophils in multiple-dosed mice. Formation of eosinophil-rich granulomas and airway goblet cell metaplasia were prevalent in the lungs of multiple-dosed mice but not in single- or saline-dosed groups. Researchers detected changes in the cytokine expression profiles in both the BAL and plasma. Multiple pulmonary exposures to S. chartarum induced significant metabolic changes in the lungs but not in the plasma. These changes suggest a shift from type 1 inflammation after an acute exposure to type 2 inflammation after multiple exposures to S. chartarum. Eotaxin, vascular endothelial growth factor (VEGF), MIP-1α, MIP-1β, TNF-α, and the IL-8 analogs macrophage inflammatory protein-2 (MIP-2) and keratinocyte chemoattractant (KC), had more dramatic changes in multiple- than in single-dosed mice, and parallel the cytokines that characterize humans with histories of mold exposures versus unexposed control subjects.
Bae HK, Shinozuka J, Islam Z, Pestka JJ. Satratoxin G interaction with 40S and 60S ribosomal subunits precedes apoptosis in the macrophage. Toxicology and applied pharmacology. 2009;237:137–145. PMID: 19306889
Satratoxin G (SG) and other macrocyclic trichothecene mycotoxins are potent inhibitors of eukaryotic translation that are potentially immunosuppressive. The purpose of this research was to test the hypothesis that SG-induced apoptosis in the macrophage correlates with binding of this toxin to the ribosome. SG rapidly binds small and large ribosomal subunits in a concentration- and time-dependent manner that was consistent with induction of apoptosis.
Edmondson DA, Barrios CS, Brasel TL, Straus DC, Kurup VP, Fink JN. Immune response among patients exposed to molds. International journal of molecular sciences. 2009;10:5471–5484. PMID: 20054481
Cellular and humoral immune responses and the presence of trichothecenes were evaluated in patients with mold-related health complaints. T-cell proliferation, macrocyclic trichothecenes, and mold specific IgG and IgA levels were not significantly different than controls; however 70% of the patients had positive skin tests to molds. Thus, IgE mediated or other non-immune mechanisms could be the cause of their symptoms.
Hellgren UM, Leino M, Aarnisalo AA, Mussalo-Rauhamaa H, Alenius H, Reijula K. Low tumor necrosis factor alpha levels and neutrophil counts in nasal lavage after mold exposure. Annals of allergy, asthma & immunology. 2009;102:210–215. PMID: 19354067
This study investigated local inflammatory responses after mold exposure in the upper respiratory tract and the feasibility of nasal lavage in diagnosing work-related exposure. The results suggest that exposure to toxin-producing microbial growth in a water-damaged building caused immunosuppression in nasal mucosa, leading to a decrease in neutrophil counts and tumor necrosis factor alpha levels.
Kankkunen P, Rintahaka J, Aalto A, Leino M, Majuri ML, Alenius H, Wolff H, Matikainen S. Trichothecene mycotoxins activate inflammatory response in human macrophages. J Immunol. 2009 May 15;182(10):6418-25. PMID: 19414795
In this report, we have examined the effect of S. chartarum and trichothecene mycotoxins on the proinflammatory cytokine response in human macrophages. Our results indicate that human macrophages sense trichothecene mycotoxins as a danger signal, which activates caspase-1, and further enables the secretion of IL-1beta and IL-18 from the LPS-primed cells.
Wang H, Yadav JS. DNA damage, redox changes, and associated stress inducible signaling events underlying the apoptosis and cytotoxicity in murine alveolar macrophage cell line MH-S by methanol-extracted Stachybotrys chartarum toxins. Toxicology and applied pharmacology. 2006;214:297–308. PMID: 16476459
Spore-extracted toxins of the indoor mold Stachybotrys chartarum (SC) caused cytotoxicity (release of lactate dehydrogenase), inhibition of cell proliferation, and cell death in murine alveolar macrophage cell line MH-S in a dose- and time-dependent manner. The study constitutes the first report on induction of DNA damage and associated p53 activation by SC toxins, and demonstrates the involvement of p38- and p53-mediated signaling events in SC toxin-induced apoptosis of alveolar macrophages.
Hymery N, Sibiril Y, Parent-Massin D. In vitro effects of trichothecenes on human dendritic cells. Toxicology in vitro : an international journal published in association with BIBRA. 2006;20:899–909. PMID: 16517116
The aim of this work was to study the in vitro effects of trichothecenes on human dendritic cells. The results suggest trichothecenes have adverse effects on dendritic cells and dendritic cell maturation process.
Chung YJ, Yang GH, Islam Z, Pestka JJ. Up-regulation of macrophage inflammatory protein-2 and complement 3A receptor by the trichothecenes deoxynivalenol and satratoxin G. Toxicology. 2003;186:51–65. PMID: 12604170
Differential display analysis was applied to assess the effects of the trichothecenes deoxynivalenol (vomitoxin, DON) and satratoxin G (SG), on mRNA in the RAW 264.7 macrophage cell line. Both MIP-2 and C3aR mRNAs were up-regulated by DON while only MIP-2 mRNA was induced by SG. MIP-2 protein was also found to be induced by both DON and SG in RAW 264.7 cell cultures.
Nielsen KF, Huttunen K, Hyvärinen A, Andersen B, Jarvis BB, Hirvonen MR. Metabolite profiles of Stachybotrys isolates from water-damaged buildings and their induction of inflammatory mediators and cytotoxicity in macrophages. Mycopathologia. 2002;154:201–205. PMID: 12206322
The metabolite profiles of 20 Stachybotrys spp. isolates from Finnish water-damaged buildings were compared with their biological activities. Effects of purified compounds on cytotoxicity and production of inflammatory mediators such as nitric oxide, IL-6 and TNFalpha in murine RAW264.7 macrophage cells were studied. The 11 isolates belonging to the satratoxin-producing chemotype were highly cytotoxic to the macrophages. The isolates inducing inflammatory mediators all belonged to the atranone-producing chemotype, but pure atranones B, and D did not elicit a response in the bioassay.
Johanning E, Biagini R, Hull D, Morey P, Jarvis B, Landsbergis P. Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office environment. International archives of occupational and environmental health. 1996;68:207–218. PMID: 8738349
The objective of this study was to evaluate the health status of office workers after exposure to fungal bio-aerosols, especially Stachybotrys chartarum (atra) (S. chartarum) and its toxigenic metabolites (satratoxins), and to study laboratory parameters or biomarkers related to allergic or toxic human health effects. Strong associations with exposure indicators and significant differences between employees (n = 53) and controls (n = 21) were found for lower respiratory system symptoms, dermatological symptoms, eye symptoms, constitutional symptoms, chronic fatigue symptoms and several enumeration and function laboratory tests, mainly of the white blood cell system. The proportion of mature T-lymphocyte cells (CD3%) was lower in employees than in controls, and regression analyses showed significantly lower CD3% among those reporting a history of upper respiratory infections.
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