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Updated: Aug 30, 2026

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
Commensal bacteria increase invasion of intestinal epithelium by Salmonella enterica serovar Typhi
1The Channing Laboratory, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA. jlyczak@channing.harvard.edu
Abstract:
The intestinal microflora consists of a heterogeneous population of microorganisms and has many effects on the health status of its human host. Here, it is shown that the products of certain strains of bacteria normally present in the intestinal microflora are able to trigger redistribution of the cystic fibrosis transmembrane conductance regulator (CFTR) protein in epithelial cells. CFTR is used by Salmonella enterica serovar Typhi as a receptor on epithelial cells which mediate the translocation of this microorganism to the gastric submucosa. Serovar Typhi-epithelial cell adhesion and CFTR-dependent invasion by serovar Typhi of epithelial cells were increased following commensal-mediated CFTR redistribution. These data suggest that commensal microorganisms present in the intestinal lumen can affect the efficiency of serovar Typhi invasion of the intestinal submucosa. This could be a key factor influencing host susceptibility to typhoid fever.
Insights
Gut bacteria products can alter cystic fibrosis transmembrane conductance regulator (CFTR) protein distribution, increasing Salmonella Typhi invasion and potentially influencing typhoid fever susceptibility.
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- The intestinal microflora comprises diverse microorganisms impacting host health.
- The cystic fibrosis transmembrane conductance regulator (CFTR) protein plays a role in epithelial cell function.
Purpose of the Study:
- To investigate how commensal gut bacteria influence the interaction between epithelial cells and Salmonella enterica serovar Typhi.
- To determine if bacterial products can alter CFTR protein localization and affect pathogen invasion.
Main Methods:
- Analysis of CFTR protein redistribution in epithelial cells induced by commensal bacterial products.
- Assessment of Salmonella Typhi adhesion and invasion following CFTR redistribution.
Main Results:
- Products from certain intestinal bacteria trigger CFTR protein redistribution in epithelial cells.
- This redistribution enhances Salmonella Typhi adhesion and invasion, utilizing CFTR as a receptor.
- Commensal-mediated CFTR changes increase pathogen translocation to the gastric submucosa.
Conclusions:
- Commensal microorganisms can modulate epithelial cell CFTR protein, impacting Salmonella Typhi invasion efficiency.
- This interaction may be a critical factor in host susceptibility to typhoid fever.
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