scispace - formally typeset
C

Carrie A. Cowardin

Researcher at University of Virginia

Publications -  17
Citations -  957

Carrie A. Cowardin is an academic researcher from University of Virginia. The author has contributed to research in topics: Clostridium difficile & Immune system. The author has an hindex of 12, co-authored 14 publications receiving 669 citations. Previous affiliations of Carrie A. Cowardin include Washington University in St. Louis & University of Virginia Health System.

Papers
More filters
Journal ArticleDOI

Effects of microbiota-directed foods in gnotobiotic animals and undernourished children

TL;DR: Identifying ingredients in complementary foods, consumed during the transition from exclusive milk feeding to a fully weaned state, that increase the representation and expressed beneficial functions of growth-promoting bacterial taxa in the developing microbiota could provide an effective, affordable, culturally acceptable, and sustainable approach to treatment.
Journal ArticleDOI

Microbiota-Regulated IL-25 Increases Eosinophil Number to Provide Protection during Clostridium difficile Infection

TL;DR: Findings support a mechanism whereby the induction of IL-25-mediated eosinophilia can reduce host mortality during active CDI, and may provide targets for future development of microbial or immune-based therapies.
Journal ArticleDOI

Bone Marrow Dendritic Cells from Mice with an Altered Microbiota Provide Interleukin 17A-Dependent Protection against Entamoeba histolytica Colitis

TL;DR: It is demonstrated that intestinal colonization with a specific commensal bacterium can provide protection during amebiasis in a murine model and that the microbiome can mediate protection against an enteric infection via extraintestinal effects on bone marrow-derived dendritic cells.
Journal ArticleDOI

IL-33 drives group 2 innate lymphoid cell-mediated protection during Clostridium difficile infection

TL;DR: It is demonstrated that IL-33 prevents C. difficile-associated mortality and epithelial disruption independently of bacterial burden or toxin expression, andIL-33 signaling to ILC2s is an important mechanism of defense from C.difficile colitis.