The Effect of Sphingosine 1-Phosphate/Sphingosine 1-Phosphate Receptor on Neutrophil Function and the Relevant Signaling Pathway

2015 ◽  
Vol 134 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Zhongying Wang ◽  
Huahua Fan ◽  
Rufeng Xie ◽  
Jie Yang ◽  
Yana Ren ◽  
...  

Background/Aims: This study investigated the priming effect of sphingosine 1-phosphate (S1P) on formyl-Met-Leu-Phe-OH (fMLP)-activated neutrophils, by specific analysis of the neutrophil respiratory burst and the signaling pathway involved in S1P activity. Methods: The neutrophil respiratory burst was indirectly detected by the cytochrome c reduction method and the dihydrorhodamine 123 staining method. The signal transduction pathways of neutrophil respiratory burst primed by S1P were detected by Western blotting. Results: Our results showed that the S1P receptors (S1PRs) 1, 4 and 5 were the predominantly expressed neutrophil S1PRs at the cDNA level. After pretreatment with S1P, the fMLP-activated neutrophils released increased levels of superoxide anions. PI3K and Akt proteins were involved in the signaling pathway of the neutrophil respiratory burst primed by S1P. Conclusion: The results indicate that S1P is a new priming reagent for neutrophils and primes the respiratory burst of fMLP-activated neutrophils. S1P interacts with its receptors on neutrophils, resulting in NADPH oxidase activation by the PI3K-Akt cell signaling pathway and induction of the neutrophil respiratory burst.

2007 ◽  
Vol 293 (5) ◽  
pp. L1293-L1299 ◽  
Author(s):  
Mitchell R. White ◽  
Tesfaldet Tecle ◽  
Erika C. Crouch ◽  
Kevan L. Hartshorn

Surfactant protein D (SP-D) and neutrophils participate in the early innate immune response to influenza A virus (IAV) infection. SP-D increases neutrophil uptake of IAV and modulates neutrophil respiratory burst responses to IAV; however, neutrophil proteases have been shown to degrade SP-D, and human neutrophil peptide defensins bind to SP-D and can cause precipitation of SP-D from bronchoalveolar lavage fluid (BALF). BALF has significant antiviral activity against IAV. We first added neutrophils to BALF during incubation with IAV. Addition of neutrophils to BALF caused significantly greater clearance of IAV from culture supernatants than from BALF alone, and this effect was significantly more pronounced when neutrophils were activated during incubation with the virus. In contrast, if activated neutrophils were incubated with BALF before addition of virus, they reduced antiviral activity of BALF. This effect correlated with depletion of SP-D from BALF. Activation of neutrophils with agonists that induce primary granule release (including release of human neutrophil peptide defensins) caused SP-D depletion, but activation with PMA, which causes only secondary granule release, did not. The ability of activated neutrophils to deplete SP-D from BALF was partially, but not fully, corrected with protease inhibitors but was unaffected by inhibition of neutrophil respiratory burst responses. These results suggest that chronic neutrophilic inflammation (e.g., as in chronic smoking or cystic fibrosis) may reduce SP-D levels and predispose to IAV infection. In contrast, acute inflammation, as occurs in the early phase of IAV infection, may promote neutrophil-mediated viral clearance.


1984 ◽  
Vol 259 (21) ◽  
pp. 13166-13171
Author(s):  
T G Gabig ◽  
B A Lefker ◽  
P J Ossanna ◽  
S J Weiss

2010 ◽  
Vol 82 (5) ◽  
pp. 876-887 ◽  
Author(s):  
Kathrin A. Dunlap ◽  
Hyeong-il Kwak ◽  
Robert C. Burghardt ◽  
Fuller W. Bazer ◽  
Ronald R. Magness ◽  
...  

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
María Mercedes Romero ◽  
Juan Ignacio Basile ◽  
Beatriz López ◽  
Viviana Ritacco ◽  
Lucía Barrera ◽  
...  

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