Salmonella typhi uses CFTR to enter intestinal epithelial cells

@article{Pier1998SalmonellaTU,
  title={Salmonella typhi uses CFTR to enter intestinal epithelial cells},
  author={Gerald B. Pier and Martha Grout and Tanweer S Zaidi and Gloria Meluleni and Simone Mueschenborn and George S Banting and Rosemary Ratcliff and Martin John Evans and William Henry Colledge},
  journal={Nature},
  year={1998},
  volume={393},
  pages={79-82}
}
Homozygous mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis (CF. [] Key Result Cells expressing wild-type CFTR internalized more S. typhi than isogenic cells expressing the most common CFTR mutation, a phenylalanine deleted at residue 508 (Δ508). Monoclonal antibodies and synthetic peptides containing a sequence corresponding to the first predicted extracellular domain of CFTR inhibited uptake of S. typhi.
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368 Citations

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Resistance to typhoid fever
Salmonella enterica Serovar Typhi Modulates Cell Surface Expression of Its Receptor, the Cystic Fibrosis Transmembrane Conductance Regulator, on the Intestinal Epithelium
TLDR
It is suggested that serovar Typhi induces intestinal epithelial cells to increase membrane CFTR levels, leading to enhanced bacterial ingestion and submucosal translocation, which could be a key, early step in the infectious process leading to typhoid fever.
Type IV(B) pili are required for invasion but not for adhesion of Salmonella enterica serovar Typhi into BHK epithelial cells in a cystic fibrosis transmembrane conductance regulator-independent manner.
Impact of Heterogeneity within Cultured Cells on Bacterial Invasion: Analysis of Pseudomonas aeruginosa andSalmonella enterica Serovar Typhi Entry into MDCK cells by Using a Green Fluorescent Protein-Labelled Cystic Fibrosis Transmembrane Conductance Regulator Receptor
TLDR
Within a population of MDCK–GFP-CFTR cells, there are cells with markedly different abilities to ingest bacteria via CFTR, and overexpression of the CFTR receptor does not increase total bacterial uptake but rather allows more epithelial cells to ingest fewer total bacteria.
Susceptibility to typhoid fever is associated with a polymorphism in the cystic fibrosis transmembrane conductance regulator (CFTR)
TLDR
The association between genotypes in CFTR and susceptibility to typhoid fever is found and analyses suggest that the role CFTR plays in vitro in S. typhi infection is also important for infection in the human population.
Role of Cystic Fibrosis Transmembrane Conductance Regulator in Pulmonary Clearance of Pseudomonas aeruginosa In Vivo1
TLDR
The results indicate that there is no direct correlation between levels of CFTR expression and bacterial clearance or association of bacteria with epithelial cells in vivo.
Cystic Fibrosis Transmembrane Conductance Regulator-Mediated Corneal Epithelial Cell Ingestion of Pseudomonas aeruginosaIs a Key Component in the Pathogenesis of Experimental Murine Keratitis
TLDR
In experimental murine eye infections, multiple additions of 5 nM CFTR peptide 103-117 to inocula of either cytotoxic (exoU+) or noncytotoxic P. aeruginosa resulted in large reductions in bacteria in the eye and markedly lessened eye pathology.
Expression of ΔF508 Cystic Fibrosis Transmembrane Regulator (CFTR) Decreases Membrane Sialylation
TLDR
It is determined that ΔF508 CFTR is associated with decreased membrane sialic acid residues in the α2, 3 position and increased concentrations of asialo- GM1, and this change occurs during post-translational modification of glycoproteins and glycolipids.
Distribution of CFTR variations in an Indonesian enteric fever cohort.
TLDR
A correlation exists between variations in the CFTR gene and protection from enteric fever, and the IVS8CA polymorphism that was identified previously may be the principal functional variation causing the difference in susceptibility.
CFTR is required for cellular entry and internalization of Chlamydia trachomatis
TLDR
It is reported that CFTR (cystic fibrosis transmembrane conductance regulator), an apical epithelial anion channel, is required for cellular entry and internalization of C. trachomatis and these findings may lead to the development of new treatment strategies to curtail the spread of chlamydial infections.
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