E
Elaine Tuomanen
Researcher at St. Jude Children's Research Hospital
Publications - 271
Citations - 22787
Elaine Tuomanen is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Streptococcus pneumoniae & Pneumococcal infections. The author has an hindex of 75, co-authored 269 publications receiving 21745 citations. Previous affiliations of Elaine Tuomanen include Rockefeller University & University of Virginia.
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Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2
Atsutoshi Yoshimura,Egil Lien,Robin R. Ingalls,Elaine Tuomanen,Roman Dziarski,Douglas T. Golenbock +5 more
TL;DR: The similarity of clinical response to invasive infection by Gram-positive and Gram-negative bacteria is due to bacterial recognition via similar TLRs, and a soluble preparation of peptidoglycan prepared from S. aureus was tested.
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Targeted disruption of the p50 subunit of NF-κB leads to multifocal defects in immune responses
TL;DR: Data support the role of NF-kappa B as a vital transcription factor for both specific and nonspecific immune responses, but do not indicate a developmental role for the factor.
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Streptococcus pneumoniae anchor to activated human cells by the receptor for platelet-activating factor
TL;DR: It is shown that inflammatory activation of human cells shifts the targeting of the pneumococcus to a new receptor, that for the G-protein-coupled platelet-activating factor (PAF) and this progression could be arrested in vitro and in vivo by PAF-receptor-specific antagonists, suggesting a possible approach to therapy.
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Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens
Karim C. El Kasmi,Joseph E. Qualls,John T. Pesce,Amber M. Smith,Robert W. Thompson,Marcela Henao-Tamayo,Randall J. Basaraba,Till König,Ulrike Schleicher,Mi-Sun Koo,Gilla Kaplan,Katherine A. Fitzgerald,Elaine Tuomanen,Ian M. Orme,Thirumala-Devi Kanneganti,Christian Bogdan,Thomas A. Wynn,Peter J. Murray +17 more
TL;DR: A 'loophole' in the TLR pathway that is advantageous to intracellular pathogens is reported that favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection.
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The rate of killing of Escherichia coli by beta-lactam antibiotics is strictly proportional to the rate of bacterial growth.
TL;DR: Slow growing bacteria became progressively more phenotypically tolerant to beta-lactam antibiotics as the generation time was extended, and all killing rates were a constant function of the bacterial generation time.