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Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages
Published on: May 30, 2013
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Proteomic analysis of the host-pathogen interface in experimental cholera.
Abdelrahim Zoued1,2,3, Hailong Zhang1,2,3, Ting Zhang1,2
1Division of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.
Nature Chemical Biology
|October 22, 2021
Summary
Cholera toxin coats Vibrio cholerae with host proteins, including SP-D, impacting infection. Host proteins on bacteria suggest roles in gut homeostasis and defense.
Area of Science:
- Microbiology
- Immunology
- Host-Pathogen Interactions
Background:
- Microbe-host interactions at the cell surface are crucial for infection outcomes.
- Identifying host proteins at this interface is challenging.
Purpose of the Study:
- To identify and quantify host proteins on Vibrio cholerae surfaces during cholera infection.
- To understand the role of specific host proteins in V. cholerae colonization and host defense.
Main Methods:
- Surface biotinylation coupled with quantitative mass spectrometry.
- Utilized an infant rabbit model of cholera.
- Investigated gene expression changes (transcriptomes) in host and pathogen.
Main Results:
- Vibrio cholerae surfaces were coated with host proteins, influenced by cholera toxin.
- The C-type lectin SP-D was identified on V. cholerae; SP-D deficient mice showed increased colonization.
- Other host proteins (AnxA1, LPO, ZAG) binding V. cholerae also recognized gut microbiota, indicating roles in homeostasis.
Conclusions:
- Cholera toxin drives host protein coating on V. cholerae, affecting colonization.
- SP-D plays a role in controlling V. cholerae intestinal colonization.
- Host proteins binding bacteria may regulate gut microbiota and maintain intestinal homeostasis.
