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Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Active modification of host inflammation by Salmonella
Ana Victoria C Pilar1, Sarah A Reid-Yu, Colin A Cooper
1Michael G. DeGroote Institute for Infectious Disease Research and the Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Canada.
Gut Microbes
|January 22, 2013
Summary
Salmonella enterica uses the effector GogB to dampen host immunity by blocking NFκB activation, reducing gut inflammation and tissue damage during chronic infections.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Salmonella enterica pathogenesis involves dampening host immune responses.
- The secreted effector GogB is implicated in Salmonella's evasion strategies.
Purpose of the Study:
- To summarize recent findings on GogB's role in disrupting NFκB activation.
- To discuss the implications of GogB in host-pathogen interactions.
Main Methods:
- Investigated the interaction of GogB with host factors Skp1 and FBXO22.
- Analyzed the effect of GogB on IκB degradation and NFκB pathway activation.
Main Results:
- GogB prevents IκB degradation by the host SCF E3 ubiquitin ligase via Skp1 and FBXO22.
- This interaction inhibits NFκB activation, dampening the host inflammatory response.
Conclusions:
- GogB is a key Salmonella effector that suppresses host immunity.
- Understanding GogB's mechanism provides insights into host-pathogen interactions and potential therapeutic targets.
