Unno Hiromichi, Kamei Katsuhiko, Honda Akira, Nishimura Kazuko, Kuriyama Takayuki
Department of Chest Medicine School of Medicine, Chiba University, Chiba, Japan.
J Infect Chemother. 2005 Jun;11(3):136-40. doi: 10.1007/s10156-005-0382-2.
Schizophyllum commune has recently emerged as a causative agent of human mycosis, but the details of its virulence are not yet known. To elucidate the pathogenicity of S. commune, a murine model of invasive pulmonary infection was established. ICR mice, not immunosuppressed or immunosuppressed by cortisone acetate, were infected with S. commune by intratracheal inoculation with agar beads containing the basidiospores. All immunosuppressed mice died within 2 weeks. Pathology examination revealed massive mycelial invasion into the lungs, penetration into adjacent vessels, and systemic dissemination, suggesting much higher virulence of this fungus than was previously estimated. This is the first murine model of pulmonary infection by S. commune, which we believe can be of assistance during subsequent investigations of this infection.
裂褶菌最近已成为人类真菌病的病原体,但其毒力细节尚不清楚。为阐明裂褶菌的致病性,建立了侵袭性肺部感染的小鼠模型。通过气管内接种含有担孢子的琼脂珠,将未免疫抑制或经醋酸可的松免疫抑制的ICR小鼠感染裂褶菌。所有免疫抑制小鼠在2周内死亡。病理检查显示大量菌丝侵入肺部,穿透至相邻血管并发生全身播散,提示该真菌的毒力比先前估计的要高得多。这是首个裂褶菌肺部感染的小鼠模型,我们认为它可在后续该感染的研究中发挥作用。