Intranasal exposure to a damp building mould, Stachybotrys chartarum, induces lung inflammation in mice by satratoxin‐independent mechanisms

@article{Leino2003IntranasalET,
  title={Intranasal exposure to a damp building mould, Stachybotrys chartarum, induces lung inflammation in mice by satratoxin‐independent mechanisms},
  author={Marika Leino and Mika J M{\"a}kel{\"a} and Kari E. Reijula and Tari Haahtela and Helena Mussalo-Rauhamaa and Tapani Tuomi and E L Hintikka and Harri Alenius},
  journal={Clinical \& Experimental Allergy},
  year={2003},
  volume={33}
}
Background Stachybotrys chartarum is a damp building mould and a potent toxin producer that has been related to serious cases of respiratory health problems. However, the direct link between exposure and health symptoms has not been established. 
Intranasal exposure to Stachybotrys chartarum enhances airway inflammation in allergic mice.
TLDR
Exposure to S. chartarum modulates the inflammatory reaction and airway hyperresponsiveness, depending on the allergic status of the exposed mice.
Acute inflammatory responses to Stachybotrys chartarum in the lungs of infant rats: time course and possible mechanisms.
TLDR
The difference between autoclaved and intact spores indicates the involvement of fungal proteins in the inflammatory response to S. chartarum and sheds new light on the clinical importance of "nontoxic" strains.
Stachybotrys chartarum, trichothecene mycotoxins, and damp building-related illness: new insights into a public health enigma.
TLDR
Solving the enigma of whether Stachybotrys inhalation indeed contributes to DBRI will require studies of the pathophysiologic effects of low dose chronic exposure to well-characterized, standardized preparations of S. chartarum spores and mycelial fragments, and, coexposures with other environmental cofactors.
Pulmonary effects of Stachybotrys chartarum in animal studies.
TLDR
Animal studies to date support the view that pulmonary exposure to the spores of S. chartarum leads to hemorrhagic inflammation and impairment of growth and indicate that lower doses, closer to the concentrations encountered in indoor air, can elicit similar symptoms.
Comparison of Inflammatory Responses in Mouse Lungs Exposed to Atranones A And C from Stachybotrys Chartarum
TLDR
It is suggested that atranones are inflammatory but also that they exhibit different inflammatory potency with different toxicokinetics, and exposure to these toxins in spores of S. chartarum in contaminated building environments could contribute to inflammatory lung disease onset in susceptible individuals.
A Quantitative Risk Assessment for Stachybotrys chartarum- Toxic Mold
TLDR
This study suggests that S. chartarum exposure via inhalation in residential conditions may pose a risk for AIPH resulting in mortality in human infants, but a conclusive epidemiological study is needed to validate risk estimates.
The role of fungal proteinases in pathophysiology of Stachybotrys chartarum
TLDR
Results suggest that proteinases from S. chartarum spores significantly contribute to lung inflammation and injury.
Trichothecene Mycotoxins Activate Inflammatory Response in Human Macrophages1
TLDR
Results indicate that human macrophages sense trichothecene mycotoxins as a danger signal, which activates caspase-1, and further enables the secretion of IL-1β and IL-18 from the LPS-primed cells.
The Pathogenicity of Stachybotrys chartarum.
  • E. Ochiai, K. Kamei, +4 authors A. Ando
  • Biology, Medicine
    Nihon Ishinkin Gakkai zasshi = Japanese journal of medical mycology
  • 2005
TLDR
The results suggest that inhalation of conidia may cause serious damage to the human lung, particularly when repeated, as using multiple injections during a 3-week period showed strong eosinophilic infiltration into the proximal alveoli and perivascular tissues.
Comparison Of Immunomodulator mRNA and Protein Expression in the Lungs of Stachybotrys chartarum Spore-Exposed Mice
TLDR
Similarities in expression among all spore treatment animals suggest that chemicals other than toxic secondary metabolites, and possibly spore-sequestered 1,3-β-D-glucan, may contribute to lung pathogenesis.
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TLDR
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TLDR
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