<abstract xmlns="http://www.w3.org/1999/xhtml">

<p><italic>Yersinia</italic> species are bacterial pathogens that can cause plague and intestinal diseases after invading into human cells through the Three Secretion System (TTSS). The effect of pathogenesis is mediated by <italic>Yersinia</italic> outer proteins (Yop) and manifested as down-regulation of the cytokine genes expression by inhibiting nuclear factor-κ-gene binding (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. In addition, its pathogenesis can also manipulate the disorder of host innate immune system and cell death such as apoptosis, pyroptosis, and autophagy. Among the <italic>Yersinia</italic> effector proteins, YopB and YopD assist the injection of other virulence effectors into the host cytoplasm, while YopE, YopH, YopJ, YopO, and YopT target on disrupting host cell signaling pathways in the host cytosols. Many efforts have been applied to reveal that intracellular proteins such as Rho-GTPase, and transmembrane receptors such as Toll-like receptors (TLRs) both play critical roles in <italic>Yersinia</italic> pathogenesis, establishing a connection between the pathogenic process and the signaling response. This review will mainly focus on how the effector proteins of <italic>Yersinia</italic> modulate the intrinsic signals in host cells and disturb the innate immunity of hosts through TTSS.</p>
</abstract>

Yersinia species are bacterial pathogens that can cause plague and intestinal diseases after invading into human cells through the Three Secretion System (TTSS). The effect of pathogenesis is mediated by Yersinia outer proteins (Yop) and manifested as down-regulation of the cytokine genes expression by inhibiting nuclear factor-κ-gene binding (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. In addition, its pathogenesis can also manipulate the disorder of host innate immune system and cell death such as apoptosis, pyroptosis, and autophagy. Among the Yersinia effector proteins, YopB and YopD assist the injection of other virulence effectors into the host cytoplasm, while YopE, YopH, YopJ, YopO, and YopT target on disrupting host cell signaling pathways in the host cytosols. Many efforts have been applied to reveal that intracellular proteins such as Rho-GTPase, and transmembrane receptors such as Toll-like receptors (TLRs) both play critical roles in Yersinia pathogenesis, establishing a connection between the pathogenic process and the signaling response. This review will mainly focus on how the effector proteins of Yersinia modulate the intrinsic signals in host cells and disturb the innate immunity of hosts through TTSS.

The Functions of Effector Proteins in <italic>Yersinia</italic> Virulence

Polish Journal of Microbiology

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

The Functions of Effector Proteins in  Virulence

Yersinia species are bacterial pathogens that can cause plague and intestinal diseases after invading into human cells through the Three Secretion System...

The Functions of Effector Proteins in Yersinia Virulence

Publié en ligne: 15 mars 2016

Pages: 5 - 12

Reçu: 23 août 2015

Accepté: 25 janv. 2016

DOI: https://doi.org/10.5604/17331331.1197324

Mots clés
pathogenesis, Yops, TTSS

© 2016 LINGLIN ZHANG et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

The Functions of Effector Proteins in Yersinia Virulence

Publié en ligne: 15 mars 2016

Pages: 5 - 12

Reçu: 23 août 2015

Accepté: 25 janv. 2016

DOI: https://doi.org/10.5604/17331331.1197324

Mots cléspathogenesis, Yops, TTSS

© 2016 LINGLIN ZHANG et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Mots clés
pathogenesis, Yops, TTSS