T
Timothy S. Blackwell
Researcher at Vanderbilt University
Publications - 361
Citations - 24132
Timothy S. Blackwell is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Lung & Inflammation. The author has an hindex of 81, co-authored 316 publications receiving 20754 citations. Previous affiliations of Timothy S. Blackwell include United States Department of Veterans Affairs & University of Illinois at Chicago.
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Journal ArticleDOI
The role of nuclear factor-kappa B in cytokine gene regulation.
TL;DR: This work has shown that activation of NF-kappa B has been linked to ARDS and has been shown to be a critical proximal step in the initiation of neutrophilic inflammation in animal models.
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Pathogen-host interactions in Pseudomonas aeruginosa pneumonia.
TL;DR: In addition to antibiotic therapy, strategies directed toward enhancing host defense and/or limiting excessive inflammation could be important to improve outcome in P. aeruginosa lung infections.
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The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak.
Andrew M. Tager,Peter LaCamera,Barry S. Shea,Gabriele S. V. Campanella,Moisés Selman,Zhenwen Zhao,Vasiliy V. Polosukhin,John C. Wain,Banu A. Karimi-Shah,Nancy D. Kim,William K. Hart,Annie Pardo,Timothy S. Blackwell,Yan Xu,Jerold Chun,Andrew D. Luster +15 more
TL;DR: It is shown that lysophosphatidic acid levels increase in bronchoalveolar lavage fluid following lung injury in the bleomycin model of pulmonary fibrosis, and that mice lacking one of its receptors, LPA1, are markedly protected from fibrosis and mortality in this model.
Journal Article
In vivo antioxidant treatment suppresses nuclear factor-kappa B activation and neutrophilic lung inflammation.
Timothy S. Blackwell,Thomas R. Blackwell,Edsel P. Holden,Brian W. Christman,John W. Christman +4 more
TL;DR: The NF-kappa B pathway represents an attractive therapeutic target for strategies to control neutrophilic inflammation and lung injury and treatment with the antioxidant N-acetylcysteine 1 h before endotoxin resulted in decreased lung NF- kappa B activation in a dose-dependent manner and diminished cytokine-induced neutrophil chemoattractant mRNA expression in lung tissue.
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Sepsis and cytokines: current status.
TL;DR: A complex interaction of cytokines and cytokine-neutralizing molecules probably determines the clinical presentation and course of sepsis, and intervention in this sequence of events to modify the host inflammatory responses may prove to be a beneficial treatment strategy.