Exploiting the crosstalk between 2 immune-modulating cytokines may help combat tuberculosis (TB), reports an international team of researchers (Mayer-Barber KD et al. Nature. 2014;511:99-103). The scientists discovered that IL-1 confers host resistance to TB by stimulating lipid-derived signaling molecules known as eicosanoids that limit excessive type I interferon (IFN) production to help contain Mycobacterium tuberculosis infections.
In infected mice and patients, reduced IL-1 responses, excessive type I IFN responses, or both were linked to an imbalance of eicosanoids and to worsening of disease. Treatment with clinically approved drugs that augment levels of prostaglandin E2, an eicosanoid, promoted bacterial killing and prolonged survival in infected mice.
Hampton T. Immune Molecules Affect Tuberculosis Outcomes. JAMA. 2014;312(5):477. doi:10.1001/jama.2014.9185