scispace - formally typeset
D

David C. Laux

Researcher at University of Rhode Island

Publications -  52
Citations -  3016

David C. Laux is an academic researcher from University of Rhode Island. The author has contributed to research in topics: Escherichia coli & Mucus. The author has an hindex of 28, co-authored 52 publications receiving 2863 citations. Previous affiliations of David C. Laux include AkzoNobel & Technical University of Denmark.

Papers
More filters
Journal ArticleDOI

Carbon nutrition of Escherichia coli in the mouse intestine.

TL;DR: The results of this systematic analysis of nutrients used by E. coli MG1655 to colonize the mouse intestine are intriguing in light of the nutrient-niche hypothesis, which states that the ecological niches within the intestine are defined by nutrient availability.
Journal ArticleDOI

Glycolytic and Gluconeogenic Growth of Escherichia coli O157:H7 (EDL933) and E. coli K-12 (MG1655) in the Mouse Intestine

TL;DR: Data is presented showing that although small numbers of EDL933 grow to large numbers in the intestine in the presence of large numbers of MG1655 when both strains are fed to mice simultaneously, precolonization with MG16 55 affords protection against subsequent colonization by EDL 933, which is found both in mucus and closely associated with intestinal epithelial cells.
Journal ArticleDOI

Colonization of the streptomycin-treated mouse large intestine by a human fecal Escherichia coli strain: role of growth in mucus.

TL;DR: It is shown that when given enough time to establish a state of colonization, E. coli F-18col- persists in feces in high numbers despite subsequent challenge by E. bacteria, suggesting that the strain derived from it which does not make the E. Escherichia coli colicin can resist elimination by the latter if it is allowed enough time within the mucus layer.
Journal ArticleDOI

Role of Gluconeogenesis and the Tricarboxylic Acid Cycle in the Virulence of Salmonella enterica Serovar Typhimurium in BALB/c Mice

TL;DR: The data show that SR-11 does not require gluconeogenesis to retain full virulence and suggest that as yet unidentified sugars are utilized bySR-11 for growth during infection of BALB/c mice, and the TCA cycle operates as a full cycle.