T
Theodore J. Standiford
Researcher at University of Michigan
Publications - 313
Citations - 25021
Theodore J. Standiford is an academic researcher from University of Michigan. The author has contributed to research in topics: Cytokine & Inflammation. The author has an hindex of 92, co-authored 308 publications receiving 23406 citations. Previous affiliations of Theodore J. Standiford include University of Nebraska Medical Center.
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Journal ArticleDOI
Interleukin-8 gene expression by a pulmonary epithelial cell line. A model for cytokine networks in the lung.
Theodore J. Standiford,S L Kunkel,M A Basha,Stephen W. Chensue,J P Lynch rd,Galen B. Toews,John Westwick,Robert M. Strieter +7 more
TL;DR: Findings demonstrate potential cell-to-cell communication circuits that may be important between AMs and pulmonary epithelial cells during the recruitment phase of acute lung inflammation.
Journal ArticleDOI
Interleukin-8 (IL-8): The Major Neutrophil Chemotactic Factor in the Lung
TL;DR: In the context of the lung, the alveolar macrophage appears to play a central role by generating factors, such as interleukin-1 and tumor-necrosis factor, which are potent stimuli for the induction of IL-8 by the lung fibroblasts and type II epithelial cells.
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Enrichment of the lung microbiome with gut bacteria in sepsis and the acute respiratory distress syndrome.
Robert P. Dickson,Benjamin H. Singer,Michael W. Newstead,Nicole R. Falkowski,John R. Erb-Downward,Theodore J. Standiford,Gary B. Huffnagle +6 more
TL;DR: Culture-independent evidence is reported that the lung microbiome is enriched with gut bacteria both in a murine model of sepsis and in humans with established ARDS, potentially representing a shared mechanism of pathogenesis in these common and lethal diseases.
Journal ArticleDOI
Balance of inflammatory cytokines related to severity and mortality of murine sepsis.
Keith R. Walley,Nicholas W. Lukacs,Theodore J. Standiford,Robert M. Strieter,Steven L. Kunkel +4 more
TL;DR: Severe sepsis is associated with a largely unopposed inflammatory response, and a largelyunopposedinflammatory response (with anti-IL-10) results in severe sepsi and death, and greater anti-inflammatory mediator expression (with IL-10).
Journal ArticleDOI
The Pseudomonas aeruginosa autoinducer N-3-oxododecanoyl homoserine lactone accelerates apoptosis in macrophages and neutrophils.
Kazuhiro Tateda,Yoshikazu Ishii,Manabu Horikawa,Tetsuya Matsumoto,Shinichi Miyairi,Jean-Claude Pechère,Theodore J. Standiford,Masaji Ishiguro,Keizo Yamaguchi +8 more
TL;DR: The data suggest that the quorum-sensing molecule 3-oxo-C12-HSL has critical roles in the pathogenesis of P. aeruginosa infection, not only in the induction of bacterial virulence factors but also in the modulation of host responses.