The specificity of lethal infection was studied in noninbred white mice (age--15 to 20 and 25 to 30 days) infected intraperitoneally with the EP-2 strain of cowpox virus (CPV) in doses 10(5), 10(6) and 10(7) PFU. The virus caused the lethal infection in the 15-20-day mice; while the 25-30-day mice remained healthy and survived. Virologic, immunologic-and-histochemical and electron-microscopy examinations of the 15-20-day mice revealed a replication of the EP-2 strain in tissues bordering on the virus introduction area; there was no generalization of infection. The virus replicated first in the mesothelium cells, and after that, in fibroblasts as well as in the endothelial, fatty, adventicial, cross-striated and muscle cells and in myosatellites.
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Endogenous prostaglandin E amplifies IL-33 production by macrophages through an E prostanoid (EP)/EP-cAMP-EPAC-dependent pathway.
J Biol Chem
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Department of Medicine, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, Massachusetts 02115; Harvard Medical School, Boston, Massachusetts 02115. Electronic address:
When activated through toll-like receptors (TLRs), macrophages generate IL-33, an IL-1 family member that induces innate immune responses through ST2 signaling. LPS, a TLR4 ligand, induces macrophages to generate prostaglandin E (PGE) through inducible COX-2 and microsomal PGE synthase 1 (mPGES-1) (1). We demonstrate that IL-33 production by bone marrow-derived murine macrophages (bmMFs) requires the generation of endogenous PGE and the intrinsic expression of EP receptors to amplify NF-κB-dependent, LPS-induced IL-33 expression via exchange protein activated by cAMP (EPAC).
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Toxicol Appl Pharmacol
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School of Medicine, Fu Jen Catholic University, No. 510, Chung-Cheng Rd., Hsin-Chuang, New Taipei 24205, Taiwan; Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan City, Taiwan. Electronic address:
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Division of Cell Biology, Department of Clinical and Experimental Medicine, Linköping University, S-581 85 Linköping, Sweden. Electronic address:
From experiments in mice in which the prostaglandin E (PGE) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE was injected directly into the brain, PGE has been implicated as a mediator of inflammatory induced anorexia. Here we aimed at examining which PGE receptor (EP) that was critical for the anorexic response to peripherally injected interleukin-1β (IL-1β). However, deletion of neither EP receptor in mice, either globally (for EP, EP, and EP) or selectively in the nervous system (EP), had any effect on the IL-1β induced anorexia.
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Clin Exp Allergy
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Department of Pharmacology, Therapeutics and Toxicology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Background: Prostaglandin E2 (PGE2 ) has been proposed to exert antiasthmatic effects in patients, to prevent antigen-induced airway pathology in murine models, and to inhibit mast cells (MC) activity in vitro.
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Superior in vitro stimulation of human CD8+ T-cells by whole virus versus split virus influenza vaccines.
PLoS One
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Department of Medicine III - University Medical Center of Johannes Gutenberg-University, Mainz, Germany; Department of Medicine III - University Medical Center of Regensburg, Regensburg, Germany.
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