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Jack A. Elias

Researcher at Brown University

Publications -  335
Citations -  32637

Jack A. Elias is an academic researcher from Brown University. The author has contributed to research in topics: Inflammation & Interleukin 13. The author has an hindex of 89, co-authored 324 publications receiving 30415 citations. Previous affiliations of Jack A. Elias include Yale University & Veterans Health Administration.

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Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production

TL;DR: The targeted pulmonary expression of IL-13 causes a mononuclear and eosinophilic inflammatory response, mucus cell metaplasia, airway fibrosis, eotaxin production, airways obstruction, and nonspecific AHR in transgene-positive animals.
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IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines.

TL;DR: The results, which demonstrate for the first time that eosinophils are a potential source of IL-17 within asthmatic airways, suggest that IL- 17 might have the potential to amplify inflammatory responses through the release of proinflammatory mediators such as alpha-chemokines.
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Direct effects of interleukin-13 on epithelial cells cause airway hyperreactivity and mucus overproduction in asthma

TL;DR: The results demonstrate the importance of direct effects of IL-13 on epithelial cells in causing two central features of asthma, including airway hyperreactivity and mucus overproduction.
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Interleukin-13 Induces Tissue Fibrosis by Selectively Stimulating and Activating Transforming Growth Factor β1

TL;DR: It is demonstrated that IL-13 is a potent stimulator and activator of TGF-β1 in vivo and that this activation is mediated by a plasmin/serine protease- and MMP-9–dependent and CD44-independent mechanism and that the fibrogenic effects of IL- 13 are mediated, in great extent, by this T GF-β pathway.