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Andrew J. McDermott

Researcher at University of Michigan

Publications -  11
Citations -  529

Andrew J. McDermott is an academic researcher from University of Michigan. The author has contributed to research in topics: Chemokine & Colitis. The author has an hindex of 9, co-authored 10 publications receiving 413 citations.

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Journal ArticleDOI

The microbiome and regulation of mucosal immunity.

TL;DR: It is becoming clear that the composition and metabolic activity of the intestinal microbiome, as a whole community, exerts a profound influence on mucosal immune regulation.
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Tryptophan Catabolism Restricts IFN-γ–Expressing Neutrophils and Clostridium difficile Immunopathology

TL;DR: It is found that inhibition of tryptophan catabolism in IDO1-knockout mice led to increased mucosal destruction, cecal hemorrhage, and increased production of IFN-γ in response to C. difficile infection, but no significant change in mucosal effector or regulatory T cell numbers or IL-10 mRNA expression.
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Temporal evolution of the microbiome, immune system and epigenome with disease progression in ALS mice.

TL;DR: In this article, the authors performed a longitudinal study to simultaneously assess the gut microbiome, immunophenotype and changes in ileum and brain epigenetic marks relative to motor behavior and muscle atrophy in the mutant superoxide dismutase 1 (SOD1G93A) familial ALS mouse model.
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Interleukin-23 (IL-23), independent of IL-17 and IL-22, drives neutrophil recruitment and innate inflammation during Clostridium difficile colitis in mice.

TL;DR: Data indicate that IL‐23, but not IL‐17a or IL‐22, promotes neutrophil recruitment and inflammatory cytokine and chemokine expression in the colon in response to C. difficile infection.
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Acute infection of mice with Clostridium difficile leads to eIF2α phosphorylation and pro-survival signalling as part of the mucosal inflammatory response

TL;DR: Data underscore the local, innate, pro‐inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin‐22–pSTAT3–RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.