Growth of mycobacterium bovis (BCG) in T lymphocyte-depleted mice.

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BCG Montreal (10-6 viable bacilli) injected intravenously into adult thymectomized, irradiated, and bone marrow-reconstituted (THXB) C57Bl times C3H F1 hybrid mice induced a progressive systemic infection which killed 95% of the animals within 60 days. Control mice infected with this dose of BCG did not die. The infected THXB mice failed to develop detectable levels of tuberculin hypersensitivity although they did show considerable Arthus (3 h) reactivity. The BCG-infected THXB mice lost weight progressively, and the root spleen and root lung indices increased substantially as the infection proceeded. None of the THXB mice developed an antibacterial immune response to the systemic BCG infection, and this was reflected by the continued persistence of macroscopic lung granuloma in these animals. The BCG-infected control mice developed as many surface tubercles as did the THXB animals, but the granulomas rapidly regressed in size and numbers in the normal mice. The lung changes correlated with the amount of tritiated thymidine incorporated by the lung cells in the later stages of the BCG infection. T cell depletion depressed the early splenic peak normally seen in BCG-infected controls, but, on the other hand, there was a progressive increase in lung counts in the THXB mice as the infection progressed and this late peak was not seen in the control animals. The significance of these findings is discussed in relation to the development of antituberculous immunity by BCG-infected mice.

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