Antimicrobial cathelicidin peptide LL-37 inhibits the pyroptosis of macrophages and improves the survival of polybacterial septic mice

Simultaneous Targeting of IL-1 and IL-18 Is Required for Protection against Inflammatory and Septic Shock

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Artesunate Reduces Serum Lipopolysaccharide in Cecal Ligation/Puncture Mice via Enhanced LPS Internalization by Macrophages through Increased mRNA Expression of Scavenger Receptors

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The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response

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Antimicrobial Cathelicidin Peptide LL-37 Inhibits the LPS/ATP-Induced Pyroptosis of Macrophages by Dual Mechanism

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Plasma ATP is Required for Neutrophil Activation in a Mouse Sepsis Model

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Adenosine-5'-Triphosphate (ATP) Protects Mice against Bacterial Infection by Activation of the NLRP3 Inflammasome

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Human anti-microbial cathelicidin peptide LL-37 suppresses the LPS-induced apoptosis of endothelial cells

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Inflammasome-Dependent Release of the Alarmin HMGB1 in Endotoxemia

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Toll-like Receptor 4 Modulation as a Strategy to Treat Sepsis

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Extracellular histones are major mediators of death in sepsis

(2009) Jun Xu et al.   NATURE MEDICINE

Pyroptosis: host cell death and inflammation

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P2X7 receptor and macrophage function

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Molecular biology of inflammation and sepsis: A primer*

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