Background
In natural environments, bacteria always live in communities with others where their physiological characteristics are influenced by each other. Bacteria can communicate with one another by using autoinducers. The current knowledge on the effect of quenching bacteria on others is limited to assess the impact of quorum-quenching bacterium
Bacillus
sp. QSI-1 on proteins pattern and virulence factors production of
Aeromonas hydrophila
YJ-1
.
Proteomic analysis was performed to find out protein changes and virulence factors, after 24 h co-culture.
Results
Results showed that several proteins of
A. hydrophila
YJ-1 were altered, seventy-two differentially expressed protein spots were excised from 2-DE gels and analyzed by MALDI-TOF/TOF MS, resulting in 63 individual proteins being clearly identified from 70 spots. Among these proteins, 50 were divided into 22 classes and mapped onto 18 biological pathways. Mixed-culture growth with
Bacillus
sp. QSI-1 resulted in an increase of
A. hydrophilia
proteins involved in RNA polymerase activity, biosynthesis of secondary metabolites, flagellar assembly, and two-component systems. In contrast, mixed culture resulted in a decreased level of proteins involved in thiamine metabolism; valine, leucine and isoleucine biosynthesis; pantothenate and CoA biosynthesis. In addition, the two extracellular virulence factors, proteases and hemolysin, were significantly reduced when
A. hydrophila
was co-cultured with QSI-1, while only lipase activity was observed to increase.
Conclusions
The information gathered from our experiment showed that
Bacillus
sp. QSI-1 has a major impact on the expression of proteins, including virulence factors of
A. hydrophila
.
Electronic supplementary material
The online version of this article (10.1186/s12866-019-1515-6) contains supplementary material, which is available to authorized users.
BACKGROUND
As the main component of oral contraceptives (OCs), ethinylestradiol (EE) has been widely applied as a model drug to induce murine intrahepatic cholestasis. The clinical counterpart of EE-induced cholestasis includes women who are taking OCs, sex hormone replacement therapy, and susceptible pregnant women. Taking intrahepatic cholestasis of pregnancy (ICP) as an example, ICP consumes the medical system due to its high-risk fetal burden and the impotency of ursodeoxycholic acid in reducing adverse perinatal outcomes.
AIM
To explore the mechanisms and therapeutic strategies of EE-induced cholestasis based on the liver immune microenvironment.
METHODS
Male C57BL/6J mice or invariant natural killer T (iNKT) cell deficiency (Jα18
-/-
mice) were administered with EE (10 mg/kg, subcutaneous) for 14 d.
RESULTS
Both Th1 and Th2 cytokines produced by NKT cells increased in the liver skewing toward a Th1 bias. The expression of the chemokine/chemokine receptor Cxcr6/Cxcl16, toll-like receptors, Ras/Rad, and PI3K/Bad signaling was upregulated after EE administration. EE also influenced bile acid synthase Cyp7a1, Cyp8b1, and tight junctions ZO-1 and Occludin, which might be associated with EE-induced cholestasis. iNKT cell deficiency (Jα18
-/-
mice) robustly alleviated cholestatic liver damage and lowered the expression of the abovementioned signaling pathways.
CONCLUSION
Hepatic NKT cells play a pathogenic role in EE-induced intrahepatic cholestasis. Our research improves the understanding of intrahepatic cholestasis by revealing the hepatic immune microenvironment and also provides a potential clinical treatment by regulating iNKT cells.
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