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Strain differences influence murine pulmonary responses to Stachybotrys chartarum
Jamie H Rosenblum Lichtenstein1, Ramon M Molina, Thomas C Donaghey
1Harvard School of Public Health, Molecular and Integrative Physiological Sciences, Department of Environmental Health, 665 Huntington Ave., Building 2 Room 219, Boston, MA 02115, USA. jrosenbl@hsph.harvard.edu
Abstract:
When the fungus Stachybotrys chartarum is inhaled, its mycotoxins may cause lung injury and inflammation. The severity of human responses to S. chartarum in both occupational and home settings varies widely. To explore these differences, we intratracheally instilled C3H/HeJ, BALB/c, and C57BL/6J mice with S. chartarum spores suspended in saline. One day later, the mice were humanely killed, bronchoalveolar lavage (BAL) was performed, and biochemical and cellular indicators of lung injury and inflammation were measured. BALB/c mice showed the highest myeloperoxidase activity, albumin and hemoglobin levels, and neutrophil numbers in their BAL among the three strains. BALB/c was the only strain to show significant increases in keratinocyte-derived cytokine (KC), monocyte chemotactic protein (MCP)-1, MCP-3, macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, MIP-1gamma, MIP-2, RANTES, IL-1alpha, IL-1beta, IL-3, IL-6, IL-18, leukemia inhibitory factor, macrophage colony-stimulating factor, and TNF-alpha. A model of allergen-induced airway inflammation was examined to assess whether underlying allergic inflammation might contribute to increased susceptibility to S. chartarum-induced pulmonary inflammation and injury. Surprisingly, in BALB/c mice, ovalbumin-induced airway inflammation produced a protective effect against some S. chartarum-induced pulmonary responses. This is the first report of mammalian strain differences affecting responses to S. chartarum. These responses differ from those reported for LPS and other fungi. Analogous underlying genetic differences may contribute to the wide range of sensitivity to Stachybotrys among humans.
Insights
Genetic differences in mice influence lung inflammation responses to Stachybotrys chartarum (black mold) exposure. BALB/c mice showed heightened inflammation, suggesting similar genetic factors may explain varying human sensitivities to this mold.
Area of Science:
- Environmental Science
- Toxicology
- Immunology
Background:
- Inhaled mycotoxins from Stachybotrys chartarum (black mold) can cause lung injury and inflammation.
- Human responses to S. chartarum exposure vary significantly in different settings.
- Understanding these variations is crucial for public health and occupational safety.
Purpose of the Study:
- To investigate the impact of mammalian genetic background on pulmonary responses to S. chartarum.
- To explore potential mechanisms underlying differential susceptibility to mold-induced lung inflammation.
- To determine if pre-existing allergic airway inflammation affects susceptibility to S. chartarum.
Main Methods:
- Intratracheal instillation of S. chartarum spores into three different mouse strains (C3H/HeJ, BALB/c, C57BL/6J).
- Measurement of biochemical and cellular markers of lung injury and inflammation via bronchoalveolar lavage (BAL).
- Assessment of S. chartarum-induced inflammation in a model of ovalbumin-induced allergic airway inflammation.
Main Results:
- BALB/c mice exhibited significantly higher indicators of lung inflammation, including myeloperoxidase activity, albumin and hemoglobin levels, and neutrophil infiltration.
- BALB/c mice showed elevated levels of numerous pro-inflammatory cytokines and chemokines (KC, MCP-1, MIPs, RANTES, ILs, TNF-alpha, etc.).
- Ovalbumin-induced allergic airway inflammation unexpectedly conferred a protective effect against certain S. chartarum-induced pulmonary responses in BALB/c mice.
Conclusions:
- Significant strain-dependent differences exist in mouse responses to S. chartarum inhalation.
- These findings suggest that underlying genetic variations play a critical role in modulating susceptibility to mold-induced lung inflammation.
- The observed differences in response highlight the complexity of S. chartarum toxicity and may provide insights into human variability in sensitivity to mold exposure.
