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Updated: Jan 30, 2026

Histological Quantification to Determine Lung Fungal Burden in Experimental Aspergillosis
Published on: March 9, 2018
Studies on experimental aspergillosis in immunodeficient mice
Mice with either chemically suppressed immune response or with specifically induced T cell or B cell immunodeficiency were challenged with Aspergillus fumigatus spores. Chemical immunosuppressants used were cortisone, cyclophosphamide or silica. T cell deficiency was produced by thymectomy and ALS administration, whereas, B cell deficiency was produced by administration of anti-mouse IgM antibodies in newborn mice. The susceptibility of such animals to A. fumigatus challenge was monitored by mortality pattern and by demonstration of dissemination of fungus in different organs. The administration of cortisone or silica made mice highly susceptible to A. fumigatus infection, whereas, cyclophosphamide initially lowered host's resistance but later had little effect. Mice with B cell deficiency also did not differ significantly from normal animals. Similarly passive transfer of specific antibodies to A. fumigatus did not enhance the protection of the host to experimental aspergillosis. However, the deficiency of T cells and macrophages either alone or in combination made the animals highly susceptible to experimental aspergillosis. The results provide evidence that T cells and macrophages play essential role in immunity to murine aspergillosis. Whereas, B cell deficiency or even passive transfer of specific antibodies to A. fumigatus does not alter much the host's susceptibility to experimental aspergillosis.
Mice with either chemically suppressed immune response or with specifically induced T cell or B cell immunodeficiency were challenged with Aspergillus fumigatus spores. Chemical immunosuppressants used were cortisone, cyclophosphamide or silica. T cell deficiency was produced by thymectomy and ALS administration, whereas, B cell deficiency was produced by administration of anti-mouse IgM antibodies in newborn mice. The susceptibility of such animals to A. fumigatus challenge was monitored by mortality pattern and by demonstration of dissemination of fungus in different organs. The administration of cortisone or silica made mice highly susceptible to A. fumigatus infection, whereas, cyclophosphamide initially lowered host's resistance but later had little effect. Mice with B cell deficiency also did not differ significantly from normal animals. Similarly passive transfer of specific antibodies to A. fumigatus did not enhance the protection of the host to experimental aspergillosis. However, the deficiency of T cells and macrophages either alone or in combination made the animals highly susceptible to experimental aspergillosis. The results provide evidence that T cells and macrophages play essential role in immunity to murine aspergillosis. Whereas, B cell deficiency or even passive transfer of specific antibodies to A. fumigatus does not alter much the host's susceptibility to experimental aspergillosis.
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