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Cryopyrin activates the inflammasome in response to toxins and ATP
TLDR
It is shown that cryopyrin-deficient macrophages cannot activate caspase-1 in response to Toll-like receptor agonists plus ATP, the latter activating the P2X7 receptor to decrease intracellular K+ levels.
Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf
TLDR
Interestingly, cell death triggered by stimuli that engage caspase-1 was ablated in macrophages lacking either ASC or Ipaf, suggesting a coupling between the inflammatory and cell death pathways.
Inflammasome adaptors and sensors: intracellular regulators of infection and inflammation
TLDR
It is shown that the inflammasome is a dynamic entity that is assembled from different adaptors in a stimulus-dependent manner in response to various bacterial pathogens and tissue damage.
Macrophage‐dependent induction of the Salmonella pathogenicity island 2 type III secretion system and its role in intracellular survival
TLDR
It is concluded that SPI‐2 genes are specifically expressed upon entry into mammalian cells and are required for intracellular growth in host cells in vivo and in vitro.
Two physically, functionally, and developmentally distinct peritoneal macrophage subsets
TLDR
A new context is introduced for interpreting (and reinterpreting) data from ex vivo studies with PerC MØ diversity, development, and function, as both subsets show clear phagocytic activity and both produce nitric oxide in response to LPS stimulation in vivo.
The Salmonella invasin SipB induces macrophage apoptosis by binding to caspase-1.
TLDR
The data demonstrate that SipB functions as an analog of the Shigella invasin IpaB, and functional inhibition of caspase-1 activity by acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone blocks macrophage cytotoxicity, and macrophages lacking casp enzyme are not susceptible to Salmonella-induced apoptosis.
Critical function for Naip5 in inflammasome activation by a conserved carboxy-terminal domain of flagellin
TLDR
It is demonstrated that 35 amino acids of the carboxyl terminus of flagellin triggered inflammasome activation in the absence of bacterial contaminants or secretion systems, clarifying the molecular basis for the cytosolic response to flageLLin.
Persistent bacterial infections: the interface of the pathogen and the host immune system
TLDR
The nature of the host immune response to this type of infection and the balance between clearance of the pathogen and avoidance of damage to host tissues are discussed.
Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella
TLDR
It is shown that the NLRs NLRP3 and NLRC4 both activate caspase-1 in response to Salmonella typhimurium, and this results reveal unexpected redundancy among NLRs in host defense against intracellular pathogens in vivo.
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