ArticleCommunications biology2026
Cathepsin G and neutrophil elastase control Leishmania infantum parasitism through TLRs-dependent induction of IFN-α and TNF-α.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Leishmania infantum and Leishmania donovani are protozoan parasites that cause visceral leishmaniasis, a potentially fatal disease targeting the liver, spleen and bone marrow. To survive, these parasites manipulate host macrophage microbicidal responses and metabolic pathways. Here, we demonstrate that the host serine proteases neutrophil elastase (NE) and cathepsin G (CG), acting in concert with Toll-like receptors TLR2, TLR3, and TLR4, induce the inflammatory cytokines IFN-α and TNF-α to control L. infantum infection in macrophages. Conversely, in vivo experiments revealed that while NE and CG are necessary for inflammatory responses, including IL-12, nitric oxide, and CCL2 production, they unexpectedly promote splenic parasitism. CG-deficient mice failed to recruit Ly6C
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