Serovar Typhi Conceals the Invasion-Associated Type Three Secretion System from the Innate Immune System by Gene Regulation
Bacterial pathogens translocate effector proteins into the cytoplasm of host cells to manipulate the mammalian host. These processes, e.g. the stimulation of small regulatory GTPases, activate the innate immune system and induce pro-inflammatory responses aimed at clearing invading microbes from the infected tissue. Here we show that strict regulation of virulence gene expression can be used as a strategy to limit the induction of inflammatory responses while retaining the ability to manipulate the host. Upon entry into host tissue, Salmonella enterica serovar Typhi, the causative agent of typhoid fever, rapidly represses expression of a virulence factor required for entering tissue to avoid detection by the host innate immune surveillance. This tight control of virulence gene expression enables the pathogen to deploy a virulence factor for epithelial invasion, while preventing the subsequent generation of pro-inflammatory responses in host cells. We conclude that regulation of virulence gene expression contributes to innate immune evasion during typhoid fever by concealing a pattern of pathogenesis.
Vyšlo v časopise:
Serovar Typhi Conceals the Invasion-Associated Type Three Secretion System from the Innate Immune System by Gene Regulation. PLoS Pathog 10(7): e32767. doi:10.1371/journal.ppat.1004207
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004207
Souhrn
Bacterial pathogens translocate effector proteins into the cytoplasm of host cells to manipulate the mammalian host. These processes, e.g. the stimulation of small regulatory GTPases, activate the innate immune system and induce pro-inflammatory responses aimed at clearing invading microbes from the infected tissue. Here we show that strict regulation of virulence gene expression can be used as a strategy to limit the induction of inflammatory responses while retaining the ability to manipulate the host. Upon entry into host tissue, Salmonella enterica serovar Typhi, the causative agent of typhoid fever, rapidly represses expression of a virulence factor required for entering tissue to avoid detection by the host innate immune surveillance. This tight control of virulence gene expression enables the pathogen to deploy a virulence factor for epithelial invasion, while preventing the subsequent generation of pro-inflammatory responses in host cells. We conclude that regulation of virulence gene expression contributes to innate immune evasion during typhoid fever by concealing a pattern of pathogenesis.
Zdroje
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Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
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