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Bradley E. Britigan

Researcher at Veterans Health Administration

Publications -  89
Citations -  5126

Bradley E. Britigan is an academic researcher from Veterans Health Administration. The author has contributed to research in topics: Pseudomonas aeruginosa & Superoxide dismutase. The author has an hindex of 38, co-authored 89 publications receiving 4715 citations. Previous affiliations of Bradley E. Britigan include American Heart Association & University of Nebraska Medical Center.

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The transition metal gallium disrupts Pseudomonas aeruginosa iron metabolism and has antimicrobial and antibiofilm activity

TL;DR: Ga is investigated as a "Trojan horse" strategy that uses the transition metal gallium to disrupt bacterial Fe metabolism and exploit the Fe stress of in vivo environments and is found that Ga inhibits Pseudomonas aeruginosa growth andBiofilm formation and kills planktonic and biofilm bacteria in vitro.
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Oxidative Responses of Human and Murine Macrophages During Phagocytosis of Leishmania chagasi

TL;DR: It is demonstrated that murine and human macrophages produce O2− during phagocytosis of opsonized promastigotes and NO· each contribute to intracellular killing of L. chagasi in human and murine macrophage.
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Spin trapping evidence for myeloperoxidase-dependent hydroxyl radical formation by human neutrophils and monocytes.

TL;DR: The ability of human neutrophils and monocytes to generate hydroxyl radical through a myeloperoxidase-dependent mechanism is supported.
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Gallium Disrupts Iron Metabolism of Mycobacteria Residing within Human Macrophages

TL;DR: It is found that Ga(NO3)3 and Ga-transferrin produce an Fe-reversible concentration-dependent growth inhibition of M. tuberculosis strains and MAC grown extracellularly and within human macrophages, and this approach could have broad applicability to the study of Fe metabolism of other intracellular pathogens.
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Pseudomonas Pyocyanin Increases Interleukin-8 Expression by Human Airway Epithelial Cells

TL;DR: Increased release of IL-8, a potent neutrophil chemoattractant, in response to pyocyanin could contribute to the marked infiltration of neutrophils and subsequent neutrophIL-mediated tissue damage that are observed in Pseudomonas-associated lung disease.