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GogB Is an Anti-Inflammatory Effector that Limits Tissue Damage during Salmonella Infection through Interaction with Human FBXO22 and Skp1

PLoS Pathogens
Public Library of Science
Publication Date
DOI: 10.1371/journal.ppat.1002773
  • Research Article
  • Biology
  • Microbiology
  • Immunity
  • Inflammation
  • Bacterial Pathogens
  • Host-Pathogen Interaction
  • Microbial Growth And Development
  • Microbial Pathogens
  • Biology


Author Summary Bacterial pathogens have evolved sophisticated ways to subvert the innate defenses of their host. One way in which pathogens do so is by blocking or dampening the inflammatory response that is triggered once a microorganism is detected by the innate immune system. In this way, the microorganism can limit the activation of innate defenses in the host to promote its own colonization and dissemination. In this work we found that the enteric human pathogen Salmonella enterica serovar Typhimurium limits the activation of innate immune defenses in the host by using a bacterial protein called GogB to interfere with NFκB activation. NFκB is a key human transcription factor involved in the expression of pro-inflammatory cytokines during infection. In this infection situation, Salmonella delivers GogB to the infected cell where it interferes with ubiquitination of the NFκB inhibitor protein called IκBα to prevent translocation of NFκB to the nucleus where it would normally activate pro-inflammatory gene expression. The anti-inflammatory property of GogB is important for the bacteria to reach optimal infection densities in host tissues and to actively limit the tissue damage associated with prolonged inflammatory responses.

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