| First Author | Mattison HA | Year | 2013 |
| Journal | J Neuroimmunol | Volume | 257 |
| Issue | 1-2 | Pages | 110-5 |
| PubMed ID | 23499256 | Mgi Jnum | J:262355 |
| Mgi Id | MGI:6162390 | Doi | 10.1016/j.jneuroim.2013.02.008 |
| Citation | Mattison HA, et al. (2013) Suppressed pro-inflammatory response of microglia in CX3CR1 knockout mice. J Neuroimmunol 257(1-2):110-5 |
| abstractText | Neuronal fractalkine acts via its receptor, CX3CR1, on microglia to regulate neuroinflammation. Conflicting results have been reported in studies employing CX3CR1 deficient (Cx3cr1(-/-)) mice. Here, compared to wild-type, endotoxin-treated neuron-glial Cx3cr1(-/-)cultures produced less TNF-alpha, nitric oxide and superoxide; however, fractalkine treatment inhibited the release of pro-inflammatory factors in wild-type and BV-2 cell cultures. Furthermore, endotoxin-treated BV-2 cells expressing siRNA against CX3CR1 increased nitric oxide and TNF-alpha production. We hypothesize that CX3CL1-CX3CR1 signaling is neuroprotective and propose that the reduced production of pro-inflammatory signals in Cx3cr1(-/-)microglia may result from compensatory mechanisms and not be the direct result of CX3CR1 deficiency. |
