| First Author | Zemann B | Year | 2007 |
| Journal | Immunol Lett | Volume | 109 |
| Issue | 1 | Pages | 56-63 |
| PubMed ID | 17292973 | Mgi Jnum | J:141742 |
| Mgi Id | MGI:3819334 | Doi | 10.1016/j.imlet.2007.01.001 |
| Citation | Zemann B, et al. (2007) Normal neutrophil functions in sphingosine kinase type 1 and 2 knockout mice. Immunol Lett 109(1):56-63 |
| abstractText | Sphingosine kinase (SPHK) has been implicated as an important element in neutrophil responses to diverse stimulatory agents. To get more insight into the role of the type 1 and 2 isoforms of SPHK in neutrophil functions, we made use of the respective SPHK knockout mice. Neutrophils isolated from the bone marrow of these mice showed normal increase of intracellular Ca(2+) when stimulated in vitro by fMLP, platelet-activating factor, the anaphylatoxin C5a, or ATP, and normal migration towards fMLP and C5a. Also, recruitment of neutrophils into the peritoneum towards the chemokines KC and MIP-2 or to LPS, and into the peripheral blood after fMLP injection was similar in SPHK knockout strains and wild-type animals. An in vivo model of bacterial lung infection revealed an accelerated progression of disease in SPHK2 (but not SPHK1) knockout mice as compared to wild-type controls. However, effector functions of SPHK-deficient neutrophils, such as superoxide production, beta-glucuronidase release and their capacity to kill bacteria were unchanged as compared to wild-type cells. To conclude, the data derived from SPHK knockout mice do not support the hypothesis that any of the two lipid kinases plays a crucial role in signalling downstream of various neutrophil stimuli; SPHKs appear not to be essential for neutrophil recruitment and effector functions. |
