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The Pharmaceutical Journal Vol 267 No 7168 p470-481
6 October 2001


BPC 2001 summary


How the body resists infection by M tuberculosis

Research into the mechanisms of infection by M tuberculosis had advanced a great deal but it was not clear whether it had improved control of the disease, said Dr Jo Colstan, head of the division of mycobacterial research, the National Institute for Medical Research, London.

He presented an overview of the mechanisms by which M tuberculosis infected its host, saying that greater understanding of these might help research into new treatments for the disease.

A commonly asked question was why people who became infected with M tuberculosis could respond in completely different ways. Some died rapidly from active disease, while others never developed active TB.

M tuberculosis was a successful pathogen because it resisted exposure to toxic molecules produced by the body and altered the intracellular environment to favour its survival. However, there could be subtle differences in the immune system’s response to infection by the bacterium and these might explain differences in host response.

Dr Colstan described how M tuberculosis infected its host. The bacterium was phagocytosed into a macrophage where it might or might not be killed instantly. The infected macrophage then attracted lymphocytes and antigen-presenting cells, which presented the bacterium to alveolar T-cells. The T-cells then eliminated the bacterium using cytokine-mediated and cytotoxic responses. However, in some cases, the bacterium survived and infection continued.

He explained how this process might be thwarted by M tuberculosis. When the bacterium entered a macrophage, genes involved in recruiting other cells were activated in the macrophage. However, there was some evidence that when M tuberculosis was present in the cell, the wrong type of T-cell was attracted, which reduced the likelihood of the bacterium being destroyed.

After being phagocytosed by the macrophage, M tuberculosis was contained in a vacuole, the contents of which were acidified by the macrophage. Lysosomes then attacked the vacuole, releasing toxic substances into it. Both of these responses were attempts to kill the bacterium. However, M tuberculosis sometimes prevented the acidification of the vacuole, which prevented the lysosomes from attacking it.

“The interaction between the macrophage and the bacterium is a combination of the macrophage trying to create a toxic environment and the bacterium trying to evade it,” Dr Colstan said.

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