Shockproofing Against Sepsis

Activation of toll-like receptors by pathogens can trigger excessive release of proinflammatory cytokines that can progress to sepsis and septic shock. Researchers at the Technical University Munich now report they have stopped the cytokine storm before it begins in mice, using the simultaneous blockade of toll-like receptor 2 and toll-like receptor 4 to protect the mice against Gram-negative sepsis and septic shock.1

Companies in the space now want to see additional in vivo data in models relevant to human sepsis and called for experiments to determine whether the strategy would work against other types of sepsis.

The toll-like receptor (TLR) system recognizes a broad range of pathogens and alerts the host immune system about impending infections. But some studies have linked excessive activation of certain TLRs to sepsis, and a handful of companies are developing compounds targeting either the TLRs or downstream proinflammatory cytokines in the TLR signaling pathway such as tumor necrosis

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