10.3389/fimmu.2020.00307.s001
Shugang Qin
Shugang
Qin
Jiaxin Li
Jiaxin
Li
Chuanmin Zhou
Chuanmin
Zhou
Breanna Privratsky
Breanna
Privratsky
Jacob Schettler
Jacob
Schettler
Xin Deng
Xin
Deng
Zhenwei Xia
Zhenwei
Xia
Yong Zeng
Yong
Zeng
Hong Wu
Hong
Wu
Min Wu
Min
Wu
Data_Sheet_1_SHIP-1 Regulates Phagocytosis and M2 Polarization Through the PI3K/Akt–STAT5–Trib1 Circuit in Pseudomonas aeruginosa Infection.pdf
Frontiers
2020
Pseudomonas aeruginosa
SHIP-1
PI3K
Akt
STAT5
M1 macrophages
M2 macrophage
2020-03-18 04:12:30
Dataset
https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_SHIP-1_Regulates_Phagocytosis_and_M2_Polarization_Through_the_PI3K_Akt_STAT5_Trib1_Circuit_in_Pseudomonas_aeruginosa_Infection_pdf/11998014
<p>SHIP-1 is an inositol phosphatase that hydrolyzes phosphatidylinositol 3-kinase (PI3K) products and negatively regulates protein kinase B (Akt) activity, thereby modulating a variety of cellular processes in mammals. However, the role of SHIP-1 in bacterial-induced sepsis is largely unknown. Here, we show that SHIP-1 regulates inflammatory responses during Gram-negative bacterium Pseudomonas aeruginosa infection. We found that infected-SHIP-1<sup>−/−</sup> mice exhibited decreased survival rates, increased inflammatory responses, and susceptibility owing to elevated expression of PI3K than wild-type (WT) mice. Inhibiting SHIP-1 via siRNA silencing resulted in lipid raft aggregates, aggravated oxidative damage, and bacterial burden in macrophages after PAO1 infection. Mechanistically, SHIP-1 deficiency augmented phosphorylation of PI3K and nuclear transcription of signal transducer and activator of transcription 5 (STAT5) to induce the expression of Trib1, which is critical for differentiation of M2 but not M1 macrophages. These findings reveal a previously unrecognized role of SHIP-1 in inflammatory responses and macrophage homeostasis during P. aeruginosa infection through a PI3K/Akt–STAT5–Trib1 axis.</p>