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Proinflammatory signalling stimulated by the type III translocation factor YopB is counteracted by multiple effectors

Gloria I Viboud1, Stephane Shu Kin So, Michelle B Ryndak

  • 1Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-5222, USA.

Molecular Microbiology
|February 27, 2003
PubMed

Insights

The Yersinia type III secretion system

Area of Science:

  • Microbiology
  • Cellular Biology
  • Immunology

Background:

  • Type III secretion systems (T3SS) are crucial virulence factors for many bacterial pathogens.
  • Yersinia pseudotuberculosis utilizes T3SS to inject effector proteins (Yops) into host cells, disrupting host signaling.
  • Components of the T3SS translocation machinery, like YopB and YopD, are essential for effector delivery.

Purpose of the Study:

  • To investigate the role of T3SS translocation machinery in stimulating host proinflammatory signaling.
  • To determine how Yersinia effector proteins counteract T3SS-induced host responses.

Main Methods:

  • Infection of HeLa cells with wild-type and mutant Yersinia pseudotuberculosis strains.
  • Quantification of interleukin-8 (IL-8) production as a measure of proinflammatory signaling.
  • Analysis of host signaling pathways, including NF-κB, MAPK (ERK, JNK), and Ras activation.

Main Results:

  • A Yop-deficient mutant lacking YopE, YopH, and YopJ induced significantly higher IL-8 production compared to wild-type bacteria.
  • YopE, YopH, or YopJ alone were sufficient to counteract IL-8 production.
  • IL-8 production was dependent on YopB but not YopD, pore formation, or invasin-mediated adhesion.
  • YopB mediated the activation of NF-κB, ERK, JNK, and Ras in response to T3SS translocation.

Conclusions:

  • The Yersinia T3SS translocator protein YopB triggers a proinflammatory response upon host cell interaction.
  • Yersinia effector proteins (YopE, YopH, YopJ) act to suppress this T3SS-induced host inflammatory signaling.
  • This study elucidates a mechanism of host-pathogen interaction involving T3SS components and effector modulation of innate immunity.

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