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Antimicrobial Cathelicidin Peptide LL-37 Inhibits the LPS/ATP-Induced Pyroptosis of Macrophages by Dual Mechanism
TLDR
LL-37 potently inhibits the LPS/ATP-induced pyroptosis by both neutralizing the action of LPS and inhibiting the response of P2X7 to ATP, which may provide a novel insight into the modulation of sepsis utilizing LL-37 with a dual action on the L PS binding and P2 X7 activation.
Effects of sevoflurane and propofol on pulmonary inflammatory responses during lung resection
TLDR
One-lung ventilation induced inflammatory responses of the bronchial epithelia in the dependent lung and the nondependent lung during lung resection and this inflammatory response was significantly suppressed by sevoflurane compared with propofol.
Effects of anesthesia with sevoflurane and propofol on the cytokine/chemokine production at the airway epithelium during esophagectomy.
TLDR
Observations suggested that propofol anesthesia more potently suppresses the surgical stress-induced inflammatory perturbation at the local milieu of the airway during esophagectomy compared with sevoflurane anesthesia.
Suppressive action of resolvin D1 on the production and release of septic mediators in D-galactosamine-sensitized endotoxin shock mice.
TLDR
Observations suggest that RvD1 may be a therapeutic agent for sepsis/endotoxin shock by exerting suppressive action on the release and production of septic mediators (HMGB1 and inflammatory cytokines), the accumulation of peritoneal cells and hepatic apoptosis.
The effect of one-lung ventilation upon pulmonary inflammatory responses during lung resection
TLDR
One-lung ventilation induced inflammatory responses of the bronchial epithelia in thedependent lung and the nondependent lung during thoracic surgery, and these inflammatory responses were more augmented in the dependent lung than in the nonddependent lung.
Antimicrobial cathelicidin peptide LL-37 inhibits the pyroptosis of macrophages and improves the survival of polybacterial septic mice.
TLDR
The present findings imply that LL-37 can be a promising candidate for sepsis because of its many functions, such as the inhibition of pyroptosis, modulation of inflammatory cytokine production and antimicrobial activity.
Human Host Defense Cathelicidin Peptide LL-37 Enhances the Lipopolysaccharide Uptake by Liver Sinusoidal Endothelial Cells without Cell Activation
TLDR
A novel function of LL-37 is proposed in enhancing LPS clearance via endocytosis through the complex formation with LPS and the interaction with cell-surface heparan sulfate proteoglycans, thereby facilitating the intracellular incorporation and degradation of LPS without cell activation.
Evaluation of the effect of α-defensin human neutrophil peptides on neutrophil apoptosis.
TLDR
Observations suggest that HNPs, especially HNP-1, can not only destroy bacteria but also modulate (suppress) neutrophil apoptosis via the P2Y6 signaling pathway, which could be advantageous for the host defense against bacterial invasion.
Neutrophil extracellular traps induce IL-1β production by macrophages in combination with lipopolysaccharide
TLDR
Observations indicate that NETs induce the production of IL-1β by J774 macrophages in combination with LPS via the caspase-1 and caspasase-8 pathways, and NET-associated DNA and serine proteases are involved in NET/LPS-induced IL- 1β production as essential components.
Human anti-microbial cathelicidin peptide LL-37 suppresses the LPS-induced apoptosis of endothelial cells.
TLDR
LL-37 could suppress the LPS-induced apoptosis of endothelial cells, thereby attenuating lethal sepsis/endotoxin shock, and this study investigated the effects of LL-37 on the L PS-induced endothelial cell apoptosis in vitro and in vivo.
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