Histopathological study of murine pulmonary cryptococcosis.
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The occurrence of pulmonary cryptococcosis in humans has been recognized by a large body of clinical and pathological evidence. Primary foci of a cryptococcal infection usually appear to be established in the lung and, cryptococci then often disseminate to the central nervous system. To learn the details of the pathogenesis of pulmonary cryptococcosis, histopathological studies were carried out with mice experimentally infected with Cryptococcus neoformans through an intranasal route. This route of inoculation was chosen because it is considered to be the most common route of a human cryptococcal infection. Two clinical isolates of Cr. neoformans with different virulence were chosen and several strains of inbred mice were employed to produce the experimental models of pulmonary cryptococcosis in which a respiratory infection was induced by an intranasal instillation of saline suspension of cryptococci.When ICR mice were inoculated with yeast cells of a low-virulent, heavily encapsulated strain (TIMM 0372), nonfatal pulmonary cryptococcosis was established within one week postinfection. Histopathological studies with the infected mice revealed that numerous granulomatous lesions, containing la antigen-expressing histiocytes, developed in the lung. By contrast, in the ICR mice inoculated with yeast cells of a high-virulent, weakly encapsulated strain (TIMM 0362), fatal infection was established, involving not only the lung but also the brain and several other organs. The most prominent histopathological findings were characterized by both delay of the response of histiocytes against the invading organism in alveoli and nonsuppurative destruction of pulmonary tissue, as well as subsequent development of cerebral cystic lesions.Histopathological studies of pulmonary cryptococcosis were also carried out using murine models produced in BALB/c, C3H/He, CBA/J, DBA/2 and C57BL/6 mice. The animal models were intranasally inoculated with both strains of Cr. neoformans to develop pulmonary lesions. In result, marked proliferation of yeast cells was recognized in the lung of animals infected with either strain of Cr. neoformans. In addition, there was a tendency for the groups of animals infected with a low-virulent strain (TIMM 0372) to show more evident response of alveolar macrophages against the invading organism despite the mouse strain.The above results suggest that the variety of cryptococcal lesions produced in the lung stems from the host defense mechanism against invading cryptococci, which is determined by immunological competence of the host, on the one hand, and virulence of the infecting cryptococci, on the other. Occurrence of a histiocytic response to a certain strain of cryptococci seems to play the major role in inducing cryptococcal lesions of the lung.
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