Altering host to defeat tuberculosis

Treating patients infected with Mycobacterium tuberculosis is becoming increasingly difficult because of the emergence of multidrug-resistant bacteria. In Nature, Mayer-Barber et al. show

that it is possible to enhance the host-mediated control of M. tuberculosis by changing the innate immune response to infection. The production of type I interferons (IFN-α and IFN-β)

exacerbates infection with M. tuberculosis by inhibiting protective responses induced by signaling via IL-1. Conversely, IL-1 triggers the production of antimycobacterial cytokines and

nitric oxide and inhibits the expression of IFN-α and IFN-β. IFN-α–IFN-β and IL-1 elicit competing pathways of eicosanoid metabolism that lead to the synthesis of lipoxin or prostaglandin E2

(PGE2), respectively. The administration of either IL-1 or PGE2 improves host control of infection with M. tuberculosis in mice. Retrospective analysis of cytokine profiles from patients

with tuberculosis also shows that enhanced protection correlates with IL-1 and PGE2. Thus, it is possible to boost host control of M. tuberculosis by blocking the production of IFN-α and

IFN-β and enhancing IL-1 responses.

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