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Hayley I. Muendlein
Tufts University
PyroptosisInterferonProgrammed cell deathEffectorCell biology
3Publications
3H-index
69Citations
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Publications 5
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#1Hayley I. Muendlein (Tufts University)H-Index: 3
#2David Jetton (Tufts University)
Last. Alexander Poltorak (Tufts University)H-Index: 18
view all 7 authors...
Cell death and inflammation are interdependent host responses to infection. During pyroptotic cell death, interleukin-1β (IL-1β) release occurs through caspase-1 and caspase-11–mediated gasdermin D pore formation. In vivo, responses to lipopolysaccharide (LPS) result in IL-1β secretion. In vitro, however, murine macrophages require a second “danger signal” for the inflammasome-driven maturation of IL-1β. Recent reports have shown caspase-8–mediated pyroptosis in LPS-activated macrophages but hav...
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#1Hayley I. Muendlein (Tufts University)H-Index: 3
#2Joseph Sarhan (Tufts University)H-Index: 3
Last. Soroush Tahmasebi (McGill University)H-Index: 8
view all 13 authors...
Summary Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK signaling. However, the regulatory mechanisms underlying this kinase-dependent cytokine production remain poorly understood. In the present study, we establish that the kinase activity of RIPK1/3 regulates cytokine translation in mouse an...
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#1Joseph Sarhan (Tufts University)H-Index: 3
#2Beiyun C. Liu (Tufts University)H-Index: 6
Last. Alexander PoltorakH-Index: 18
view all 11 authors...
Interferons (IFNs) are critical determinants in immune-competence and autoimmunity, and are endogenously regulated by a low-level constitutive feedback loop. However, little is known about the functions and origins of constitutive IFN. Recently, lipopolysaccharide (LPS)-induced IFN was implicated as a driver of necroptosis, a necrotic form of cell death downstream of receptor-interacting protein (RIP) kinase activation and executed by mixed lineage kinase like-domain (MLKL) protein. We found tha...
15 CitationsSource
#1Joseph Sarhan (Tufts University)H-Index: 3
#2Beiyun C. Liu (Tufts University)H-Index: 6
Last. Alexander Poltorak (Tufts University)H-Index: 18
view all 11 authors...
Cell death and inflammation are intimately linked during Yersinia infection. Pathogenic Yersinia inhibits the MAP kinase TGFβ-activated kinase 1 (TAK1) via the effector YopJ, thereby silencing cytokine expression while activating caspase-8–mediated cell death. Here, using Yersinia pseudotuberculosis in corroboration with costimulation of lipopolysaccharide and (5Z)-7-Oxozeaenol, a small-molecule inhibitor of TAK1, we show that caspase-8 activation during TAK1 inhibition results in cleavage of bo...
35 CitationsSource
#1Beiyun C. Liu (Tufts University)H-Index: 6
#2Joseph Sarhan (Tufts University)H-Index: 3
Last. Alexander Poltorak (Tufts University)H-Index: 18
view all 9 authors...
Summary Legionella pneumophila elicits caspase-11-driven macrophage pyroptosis through guanylate-binding proteins (GBPs) encoded on chromosome 3. It has been proposed that microbe-driven IFN upregulates GBPs to facilitate pathogen vacuole rupture and bacteriolysis preceding caspase-11 activation. We show here that macrophage death occurred independently of microbial-induced IFN signaling and that GBPs are dispensable for pathogen vacuole rupture. Instead, the host-intrinsic IFN status sustained ...
19 CitationsSource
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