M
Martha Grout
Researcher at Brigham and Women's Hospital
Publications - 24
Citations - 3004
Martha Grout is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Pseudomonas aeruginosa & Antigen. The author has an hindex of 21, co-authored 23 publications receiving 2880 citations. Previous affiliations of Martha Grout include Harvard University.
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Journal ArticleDOI
Role of mutant CFTR in hypersusceptibility of cystic fibrosis patients to lung infections
Gerald B. Pier,Martha Grout,Tanweer Zaidi,John C. Olsen,Larry G. Johnson,James R. Yankaskas,Joanna B. Goldberg +6 more
TL;DR: Pseudomonas aeruginosa lipopolysaccharide (LPS)-core oligosaccharide was identified as the bacterial ligand for epithelial cell ingestion; exogenous oligosACcharide inhibited bacterial ingestion in a neonatal mouse model, resulting in increased amounts of bacteria in the lungs.
Journal ArticleDOI
Salmonella typhi uses CFTR to enter intestinal epithelial cells.
Gerald B. Pier,Martha Grout,Tanweer Zaidi,Gloria Meluleni,Simone Mueschenborn,George Banting,Rosemary Ratcliff,Martin J. Evans,William H. Colledge +8 more
TL;DR: Reduced levels of CFTR in heterozygotes may decrease susceptibility to typhoid fever, and this research finds that S. typhi, but not the related murine pathogen S. typhimurium, uses CFTR for entry into epithelial cells.
Journal ArticleDOI
Cystic fibrosis transmembrane conductance regulator is an epithelial cell receptor for clearance of Pseudomonas aeruginosa from the lung
TL;DR: It is reported that CFTR is a cellular receptor for binding, endocytosing, and clearing P. aeruginosa from the normal lung, indicating a direct connection between mutations in CFTR and the clinical consequences of CF.
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Role of Alginate O Acetylation in Resistance of Mucoid Pseudomonas aeruginosa to Opsonic Phagocytosis
Gerald B. Pier,Fadie T. Coleman,Martha Grout,Michael J. Franklin,Dennis E. Ohman,Dennis E. Ohman +5 more
TL;DR: It is shown that O acetylation of alginate maximizes the resistance of mucoid P. aeruginosa to antibody-independent opsonic killing and is the molecular basis for the Resistance to host immune effectors in CF patients.
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Acquisition of expression of the Pseudomonas aeruginosa ExoU cytotoxin leads to increased bacterial virulence in a murine model of acute pneumonia and systemic spread.
TL;DR: There was markedly increased virulence in a murine model of acute pneumonia and systemic spread because of the introduction of the exoUgene into noncytotoxic strains of P. aeruginosa lacking this gene.