scispace - formally typeset
K

Katharina Brandl

Researcher at University of Montana

Publications -  53
Citations -  3246

Katharina Brandl is an academic researcher from University of Montana. The author has contributed to research in topics: Receptor & Curriculum. The author has an hindex of 24, co-authored 46 publications receiving 2671 citations. Previous affiliations of Katharina Brandl include University of Regensburg & Memorial Sloan Kettering Cancer Center.

Papers
More filters
Journal ArticleDOI

Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits

TL;DR: It is demonstrated that antibiotic treatment of mice notably downregulates intestinal expression of RegIIIγ, a secreted C-type lectin that kills Gram-positive bacteria, including VRE, providing a potential therapeutic approach to reduce colonization and infection by antibiotic-resistant microbes.
Journal ArticleDOI

Bacteriophage targeting of gut bacterium attenuates alcoholic liver disease

TL;DR: It is shown that bacteriophages can specifically target cytolytic E. faecalis, which provides a method for precisely editing the intestinal microbiota, and is linked with more severe clinical outcomes and increased mortality in patients with alcoholic hepatitis.
Journal ArticleDOI

MyD88-mediated signals induce the bactericidal lectin RegIIIγ and protect mice against intestinal Listeria monocytogenes infection

TL;DR: It is shown that clearance of L. monocytogenes from the lumen of the distal small intestine is impaired in MyD88−/− mice, and experiments with bone marrow chimeric mice reveal that MyD 88-mediated signals in nonhematopoietic cells induce RegIIIγ expression in the small intestine, thereby enhancing bacterial killing.
Journal ArticleDOI

Additive Roles for MCP-1 and MCP-3 in CCR2-Mediated Recruitment of Inflammatory Monocytes during Listeria monocytogenes Infection

TL;DR: It is shown that L. monocytogenes infection rapidly induces MCP-3 in tissue culture macrophages and in serum, spleen, liver, and kidney following in vivo infection, suggesting that cytosolic innate immune detection mechanisms trigger chemokine production.