J
James L. Madara
Researcher at University of Chicago
Publications - 178
Citations - 24719
James L. Madara is an academic researcher from University of Chicago. The author has contributed to research in topics: Tight junction & Intestinal epithelium. The author has an hindex of 84, co-authored 178 publications receiving 24022 citations. Previous affiliations of James L. Madara include Brigham and Women's Hospital & Emory University.
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Cutting Edge: Bacterial Flagellin Activates Basolaterally Expressed TLR5 to Induce Epithelial Proinflammatory Gene Expression
TL;DR: Investigating how epithelia detect flagellin revealed that cell surface expression of Toll-like receptor 5 (TLR5) conferred NF-κB gene expression in response to flageLLin, providing a molecular basis for the polarity of this innate immune response.
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Proinflammatory Cytokines Disrupt Epithelial Barrier Function by Apoptosis-Independent Mechanisms
Matthias Bruewer,Andreas Luegering,Andreas Luegering,Torsten Kucharzik,Torsten Kucharzik,Charles A. Parkos,James L. Madara,James L. Madara,Ann M. Hopkins,Asma Nusrat +9 more
TL;DR: These findings for the first time clearly separate the proapoptotic effects of IFN-γ and TNF-α from their abilities to disrupt barrier function.
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Prokaryotic Regulation of Epithelial Responses by Inhibition of IκB-α Ubiquitination
Andrew S. Neish,Andrew T. Gewirtz,Hui Zeng,Andrew N. Young,Michael E. Hobert,Vinit Karmali,Anjali S. Rao,James L. Madara +7 more
TL;DR: The identification of enteric organisms (nonvirulent Salmonella strains) whose direct interaction with model human epithelia attenuate synthesis of inflammatory effector molecules elicited by diverse proinflammatory stimuli is reported.
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Interferon-gamma directly affects barrier function of cultured intestinal epithelial monolayers.
James L. Madara,J Stafford +1 more
TL;DR: The effects of gamma IFN on monolayer barrier function were not duplicated by the cytokine interferon 1, interleukin 2, or tumor necrosis factor, and it is speculated that such products of activation of lymphoid cells might influence barrier function of intestinal, and perhaps other epithelia in disease states.
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Regulation of the movement of solutes across tight junctions
TL;DR: It is now clear that solute permeation across tight junctions is dynamically regulated by intracellular events with a common effector mechanism apparently tied to the cytoskeleton.