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- W4313369070 abstract "Abstract NADPH oxidase 2 (Nox2) plays important roles both in protection from pathogens and in responses to inflammatory stimuli, and its functional loss is the cause of Chronic Granulomatous Disease. While earlier reports implicated macrophage Nox2 as the major contributor to inflammatory responses, we sought to determine the respective contributions of Nox2 in resident macrophages or neutrophils to early inflammatory responses induced by two different stimuli and routes of induction. We hypothesized that absence of Nox2 function in resident macrophages would drive excessive, prolonged inflammation. Intraperitoneal (i.p.) zymosan or intratracheal (i.t.) killed A. fumigatus in Nox2-deficient mice both drive a severe, sustained inflammatory response locally with continually elevated levels of neutrophils, monocytes, and macrophages and granulomata formation, whereas WT mice exhibit rapidly resolving responses. We employed a novel mixed bone marrow chimera approach in which neutrophils are predominantly Nox2-sufficient yet resident macrophages are largely Nox2-deficient. We treated these mice and WT control mixed chimeras with both i.p. zymosan and i.t. killed A. fumigatus and characterized the inflammatory response in both the lung and peritoneal cavity after either stimulus. Notably, the Nox2-deficient mixed chimeras responded similarly to WT control chimeras, including reduced neutrophil and monocyte recruitment and absence of granulomata, demonstrating that Nox2 deficiency specifically in neutrophils drives excessive inflammation in response to both i.p. zymosan and i.t. A. fumigatus. These data highlight the importance of neutrophil Nox2 in normal progression and resolution of these inflammatory responses." @default.
- W4313369070 created "2023-01-06" @default.
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- W4313369070 date "2020-05-01" @default.
- W4313369070 modified "2023-09-27" @default.
- W4313369070 title "Nox2 deficiency in neutrophils promotes excessive and sustained inflammatory responses at local and distal sites of inflammation" @default.
- W4313369070 doi "https://doi.org/10.4049/jimmunol.204.supp.148.28" @default.
- W4313369070 hasPublicationYear "2020" @default.
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