PUBLICATION

Edwardsiella piscicida type III protein EseJ suppresses apoptosis through down regulating type 1 fimbriae, which stimulate the cleavage of caspase-8

Authors
He, T.T., Zhou, Y., Liu, Y.L., Li, D.Y., Nie, P., Li, A.H., Xie, H.X.
ID
ZDB-PUB-200221-30
Date
2020
Source
Cellular Microbiology   22(7): e13193 (Journal)
Registered Authors
Nie, Pin
Keywords
Edwardsiella piscicida, apoptosis, type 1 fimbriae, type III protein EseJ
MeSH Terms
  • Animals
  • Apoptosis
  • Bacterial Proteins/metabolism*
  • Caspase 3
  • Caspase 8/metabolism*
  • Caspase 9
  • Cell Line
  • Edwardsiella/metabolism*
  • Edwardsiella/pathogenicity
  • Enterobacteriaceae Infections/metabolism
  • Epitopes
  • Fimbriae, Bacterial/metabolism*
  • Fish Diseases/microbiology
  • Host-Pathogen Interactions/physiology
  • Larva
  • Lipopolysaccharides
  • Macrophages
  • Mice
  • Type III Secretion Systems/metabolism
  • Zebrafish
PubMed
32068939 Full text @ Cell. Microbiol.
Abstract
The type III secretion system effector EseJ plays a regulatory role inside bacteria. It suppresses the adherence of Edwardsiella piscicida (E. piscicida) to host epithelial cells by down regulating type 1 fimbriae. In this study, we observed that more macrophages infected with ΔeseJ strain of E. piscicida detached as compared with those infected with the wild-type (WT) strain. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and cleaved caspase-3 examination revealed that the detachment is due to increased apoptosis, suggesting that EseJ suppresses macrophage apoptosis. However, apoptosis inhibition by EseJ is not relative to a type III secretion system (T3SS) and is not related to EseJ's translocation. Since EseJ negatively regulates type 1 fimbriae, murine J774A.1 cells were infected with ΔeseJΔfimA or ΔeseJΔfimH strains. It was demonstrated that ΔeseJ stimulates macrophage apoptosis through type 1 fimbriae. Moreover, we found that infecting J774A.1 cells with the ΔeseJ strain increased levels of cleaved caspase-8, caspase-9, and caspase-3, demonstrating that EseJ inhibits apoptosis through either an extrinsic or a combination of extrinsic and intrinsic pathways. Pretreatment of macrophages with caspase-8 inhibitor prior to infection with the ΔeseJ strain decreased the levels of cleaved caspase-8, caspase-9, and caspase-3, indicating that the ΔeseJ strain stimulates apoptosis, mainly through an extrinsic pathway by up regulating type 1 fimbriae. Zebrafish larvae or blue gourami fish infected with the ΔeseJ strain consistently exhibited higher apoptosis than those infected with the E. piscicida WT strain or ΔeseJΔfimA strain. Taken together, we revealed that the T3SS protein EseJ of E. piscicida inhibits host apoptosis, mainly through an extrinsic pathway by down regulating type 1 fimbriae. This article is protected by copyright. All rights reserved.
Genes / Markers
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes