Abstract
Summary The pathogenesis of Mycoplasma pulmonis infection was studied in normal mice and in thymectomised, X-irradiated, anti-lymphocyte-treated mice. The immunosuppressed mice were more readily infected by the intranasal route than were normal mice, although the mycoplasmas multiplied to only a slightly greater extent in the lungs of the deficient animals. Spread of mycoplasmas from the lungs to other organs, such as the brain, occurred more frequently in the immunologically deficient mice. Cell-mediated immunity appeared to be important in the development of the pulmonary lesions. Thus, the lungs of normal mice showed marked peribronchiolar and perivascular cuffing by lymphocytes, but this was much less prominent in the immunosuppressed mice and macrophages were also fewer in number. Immunofluorescence studies provided further evidence for the important role of cell-mediated immune mechanisms in M. pulmonis infections in mice. The way in which such mechanisms may operate is discussed.
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