ArticlePLoS pathogens2012
GogB is an anti-inflammatory effector that limits tissue damage during Salmonella infection through interaction with human FBXO22 and Skp1.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 94 citations in OpenAlex.
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- Comprehensive blueprint of Salmonella genomic plasticity identifies hotspots for pathogenicity genes.PLoS biology · 2024Article
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- Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria.Current opinion in immunology · 2023Review
- Mitogen-Activated Protein Kinases (MAPKs) and Enteric Bacterial Pathogens: A Complex Interplay.International journal of molecular sciences · 2023Review
- Speaking the host language: howMicrobiology (Reading, England) · 2023Review
- Antimicrobial resistance and genetic background of non-typhoidal Salmonella enterica strains isolated from human infections in São Paulo, Brazil (2000-2019).Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Bacterial pathogens often manipulate host immune pathways to establish acute and chronic infection. Many Gram-negative bacteria do this by secreting effector proteins through a type III secretion system that alter the host response to the pathogen. In this study, we determined that the phage-encoded GogB effector protein in Salmonella targets the host SCF E3 type ubiquitin ligase through an interaction with Skp1 and the human F-box only 22 (FBXO22) protein. Domain mapping and functional knockdown studies indicated that GogB-containing bacteria inhibited IκB degradation and NFκB activation in macrophages, which required Skp1 and a eukaryotic-like F-box motif in the C-terminal domain of GogB. GogB-deficient Salmonella were unable to limit NFκB activation, which lead to increased proinflammatory responses in infected mice accompanied by extensive tissue damage and enhanced colonization in the gut during long-term chronic infections. We conclude that GogB is an anti-inflammatory effector that helps regulate inflammation-enhanced colonization by limiting tissue damage during infection.
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