Research Topics
Species | B A ButcherSummaryAffiliation: Cornell University Country: USA Publications
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Publications
Larvae-induced plasma membrane wounds and glycoprotein deposition are insufficient for Trichinella spiralis invasion of epithelial cellsB A Butcher
James A Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
Mol Biochem Parasitol 107:207-18. 2000....- IL-10-independent STAT3 activation by Toxoplasma gondii mediates suppression of IL-12 and TNF-alpha in host macrophagesBarbara A Butcher
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
J Immunol 174:3148-52. 2005..gondii exploits host STAT3 to prevent LPS-triggered IL-12 and TNF-alpha production, revealing for the first time a molecular mechanism underlying the parasite's suppressive effect on macrophage proinflammatory cytokine production... - Toxoplasma gondii rhoptry kinase ROP16 activates STAT3 and STAT6 resulting in cytokine inhibition and arginase-1-dependent growth controlBarbara A Butcher
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA
PLoS Pathog 7:e1002236. 2011..We conclude that encounter between Toxoplasma ROP16 and the host cell STAT signaling cascade has pleiotropic downstream effects that act in multiple and complex ways to direct the course of infection... - Toxoplasma gondii triggers myeloid differentiation factor 88-dependent IL-12 and chemokine ligand 2 (monocyte chemoattractant protein 1) responses using distinct parasite molecules and host receptorsLaura Del Rio
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14850, USA
J Immunol 172:6954-60. 2004..gondii possesses multiple molecules triggering distinct MyD88-dependent signaling cascades, that these pathways are independently regulated, and that they lead to distinct profiles of cytokine production... - p38 MAPK autophosphorylation drives macrophage IL-12 production during intracellular infectionLeesun Kim
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 6401, USA
J Immunol 174:4178-84. 2005..Furthermore, a synthetic p38 catalytic-site inhibitor blocked tachyzoite-induced p38alpha MAPK phosphorylation. These data are the first to demonstrate p38 MAPK autophosphorylation triggered by intracellular infection... - Toxoplasma gondii interferes with lipopolysaccharide-induced mitogen-activated protein kinase activation by mechanisms distinct from endotoxin toleranceLeesun Kim
Department of Microbiology and Immunology, Cornell University College of Veterinary Medicine, Ithaca, NY 14853, USA
J Immunol 172:3003-10. 2004..Our results show that T. gondii blocks LPS-triggered cytokine production in part through MAPK inactivation, and that this occurs through pathways distinct from endotoxin-induced tolerance... - Toxoplasma gondii tachyzoites inhibit proinflammatory cytokine induction in infected macrophages by preventing nuclear translocation of the transcription factor NF-kappa BB A Butcher
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
J Immunol 167:2193-201. 2001..Our results are the first to demonstrate the ability of an intracellular protozoan to actively interfere with the NF-kappaB activation pathway in macrophages, an activity that may enable parasite survival within the host... - Mechanism of entry determines the ability of Toxoplasma gondii to inhibit macrophage proinflammatory cytokine productionBarbara A Butcher
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853 6401, USA
Infect Immun 70:5216-24. 2002..They also show that the effects of Toxoplasma on IL-12 and TNF-alpha production are nonidentical, with the parasite exerting a longer-lasting suppression of the latter... - STAT1 is essential for antimicrobial effector function but dispensable for gamma interferon production during Toxoplasma gondii infectionL Cristina Gavrilescu
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA
Infect Immun 72:1257-64. 2004.... - Toxoplasma gondii prevents chromatin remodeling initiated by TLR-triggered macrophage activationJin Leng
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
J Immunol 182:489-97. 2009.... - Toxoplasma gondii genotype determines MyD88-dependent signaling in infected macrophagesLeesun Kim
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
J Immunol 177:2584-91. 2006..Differences in host signaling pathways triggered by RH vs ME49 may contribute to the high and low virulence characteristics displayed by these parasite strains... - Dysregulation of macrophage signal transduction by Toxoplasma gondii: past progress and recent advancesJ Leng
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 6401, USA
Parasite Immunol 31:717-28. 2009..These studies reveal insight into the profound suppression of proinflammatory cytokine responses that occurs when the parasite infects macrophages and other cells of innate immunity... - Neutrophils, dendritic cells and ToxoplasmaEric Y Denkers
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 6401, USA
Int J Parasitol 34:411-21. 2004..Neutrophil-empowered dendritic cells possess properties expected of highly potent antigen presenting cells that drive T helper 1 generation... - In the belly of the beast: subversion of macrophage proinflammatory signalling cascades during Toxoplasma gondii infectionEric Y Denkers
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 6401, USA
Cell Microbiol 5:75-83. 2003..The balance of cytokine subversion and stimulation during infection probably results from the parasite's need to simultaneously avoid immune elimination and trigger immunity to prevent host death... - Sabotage and exploitation in macrophages parasitized by intracellular protozoansEric Y Denkers
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853 6401, USA
Trends Parasitol 21:35-41. 2005..The molecular details of how intracellular protozoans manipulate macrophage signal transduction pathways for their own ends are beginning to emerge... - Manipulation of mitogen-activated protein kinase/nuclear factor-kappaB-signaling cascades during intracellular Toxoplasma gondii infectionEric Y Denkers
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA
Immunol Rev 201:191-205. 2004..The balance between activation and interference with proinflammatory signaling is likely to reflect the need to achieve an appropriate level of immunity that allows the host and parasite to maintain a stable interaction... - p47 GTPases regulate Toxoplasma gondii survival in activated macrophagesBarbara A Butcher
Dept of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA
Infect Immun 73:3278-86. 2005..gondii. These results suggest that IGTP and LRG-47 are able to regulate host resistance to acute T. gondii infections through their ability to inhibit parasite growth within the macrophage... - Functional aspects of Toll-like receptor/MyD88 signalling during protozoan infection: focus on Toxoplasma gondiiC E Egan
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
Clin Exp Immunol 156:17-24. 2009..We also speculate how TLR/MyD88 signalling might be exploited to provide protection against Toxoplasma, as well as other protozoa and infection in general... - Cell wall lipids from Mycobacterium bovis BCG are inflammatory when inoculated within a gel matrix: characterization of a new model of the granulomatous response to mycobacterial componentsElizabeth R Rhoades
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
Tuberculosis (Edinb) 85:159-76. 2005..We submit that the matrix model presents pertinent features of the murine granulomatous response that will prove to be an adaptable method for study of this complex response... - Kinetics of phosphatidylinositol-3-phosphate acquisition differ between IgG bead-containing phagosomes and Mycobacterium tuberculosis-containing phagosomesGeorgiana E Purdy
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
Cell Microbiol 7:1627-34. 2005..Given the role these lipids play in the regulation of phagosome maturation these findings have implications with respect to the mechanisms behind the arrest of phagosome maturation...