Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung.
David L EbenezerPanfeng FuYashaswin KrishnanMark Maienschein-ClineHong HuSegun JungRavi MadduriZarema ArbievaAnantha HarijithViswanathan NatarajanPublished in: BMC genomics (2019)
Using Sphk2-/- mice and differential gene expression analysis, we have shown here that S1P/SPHK2 signaling could play a key role in promoting PA pneumonia. The identified genes promote inflammation and suppress others that naturally inhibit inflammation and host defense. Thus, targeting SPHK2/S1P signaling in PA-induced lung inflammation could serve as a potential therapy to combat PA-induced pneumonia.
Keyphrases
- oxidative stress
- genome wide
- genome wide identification
- diabetic rats
- pseudomonas aeruginosa
- high glucose
- drug induced
- copy number
- cystic fibrosis
- stem cells
- gene expression
- escherichia coli
- transcription factor
- climate change
- drug resistant
- mesenchymal stem cells
- endothelial cells
- adipose tissue
- multidrug resistant
- risk assessment
- insulin resistance
- bioinformatics analysis
- staphylococcus aureus
- acute respiratory distress syndrome
- human health
- acinetobacter baumannii
- replacement therapy