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.
Citation
He, T.T., Zhou, Y., Liu, Y.L., Li, D.Y., Nie, P., Li, A.H., Xie, H.X. (2020) Edwardsiella piscicida type III protein EseJ suppresses apoptosis through down regulating type 1 fimbriae, which stimulate the cleavage of caspase-8. Cellular Microbiology. 22(7):e13193.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping