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The GAP Activity of Type III Effector YopE Triggers Killing of in Macrophages


The type III secretion system (T3SS) is a macromolecular protein export pathway found in gram-negative bacteria. It delivers bacterial toxins into eukaryotic cells to promote pathogenic infection. T3SSs and the bacterial toxins delivered are critical arsenals for many bacterial pathogens of clinical significance, such as Yersinia, Salmonella and Shigella. On the other hand, the mammalian immune system may recognize the T3SS as a danger signal to signify pathogenic infection, and to stimulate appropriate defense against pathogens. Here, we show that the innate immune system recognizes the activity of YopE delivered by the Yersinia T3SS. Modulation of host Rho GTPases by YopE elicits a defensive response, which results in killing of bacteria in host cells. Inhibition of host Rho GTPases by Clostridium difficile Toxin B, another bacterial toxin, mimics the YopE-triggered killing effect. Our study demonstrates that host cells sense manipulation of Rho GTPases by bacterial toxins as a surveillance mechanism, revealing new insights into innate immune recognition of pathogenic infections.


Vyšlo v časopise: The GAP Activity of Type III Effector YopE Triggers Killing of in Macrophages. PLoS Pathog 10(8): e32767. doi:10.1371/journal.ppat.1004346
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004346

Souhrn

The type III secretion system (T3SS) is a macromolecular protein export pathway found in gram-negative bacteria. It delivers bacterial toxins into eukaryotic cells to promote pathogenic infection. T3SSs and the bacterial toxins delivered are critical arsenals for many bacterial pathogens of clinical significance, such as Yersinia, Salmonella and Shigella. On the other hand, the mammalian immune system may recognize the T3SS as a danger signal to signify pathogenic infection, and to stimulate appropriate defense against pathogens. Here, we show that the innate immune system recognizes the activity of YopE delivered by the Yersinia T3SS. Modulation of host Rho GTPases by YopE elicits a defensive response, which results in killing of bacteria in host cells. Inhibition of host Rho GTPases by Clostridium difficile Toxin B, another bacterial toxin, mimics the YopE-triggered killing effect. Our study demonstrates that host cells sense manipulation of Rho GTPases by bacterial toxins as a surveillance mechanism, revealing new insights into innate immune recognition of pathogenic infections.


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Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

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PLOS Pathogens


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