Lehmann P F, White L O
Infect Immun. 1975 Nov;12(5):987-92. doi: 10.1128/iai.12.5.987-992.1975.
Aspergillus fumigatus mycelium in untreated mice (N-mice) and cortisone acetate-treated mice (C-mice) has been quantified by chemical assay of fungal chitin. Cortisone pretreatment rendered mice more susceptible to infection by A. fumigatus (mean lethal dose at 20 days, congruent to 10(6) for N-mice; less than 10(4) for C-mice). In both N- and C-mice there was renal localization of mycelial infection at conidial doses less than the mean lethal dose. At a conidial dose greater than the mean lethal dose, mycelial infection was found in the kidneys and brain of N-mice and in the kidneys, liver, and heart of C-mice. Chitin assay results showed that A. fumigatus mycelium grew more rapidly in C-mice. It is suggested that the resistance of N-mice to mycelial development may be an important mechanism whereby natural resistance to A. fumigatus is conferred.
通过对真菌几丁质的化学分析,对未处理小鼠(N组小鼠)和醋酸可的松处理小鼠(C组小鼠)体内的烟曲霉菌丝体进行了定量分析。醋酸可的松预处理使小鼠更容易受到烟曲霉的感染(20天时的平均致死剂量,N组小鼠约为10⁶;C组小鼠小于10⁴)。在N组和C组小鼠中,当分生孢子剂量低于平均致死剂量时,菌丝体感染均定位于肾脏。当分生孢子剂量高于平均致死剂量时,在N组小鼠的肾脏和大脑以及C组小鼠的肾脏、肝脏和心脏中发现了菌丝体感染。几丁质分析结果表明,烟曲霉菌丝体在C组小鼠中生长得更快。有人提出,N组小鼠对菌丝体发育的抵抗力可能是赋予对烟曲霉天然抵抗力的重要机制。