| First Author | Klueh U | Year | 2016 |
| Journal | Biosens Bioelectron | Volume | 86 |
| Pages | 262-269 | PubMed ID | 27376197 |
| Mgi Jnum | J:350386 | Mgi Id | MGI:7625766 |
| Doi | 10.1016/j.bios.2016.06.026 | Citation | Klueh U, et al. (2016) Impact of CCL2 and CCR2 chemokine/receptor deficiencies on macrophage recruitment and continuous glucose monitoring in vivo. Biosens Bioelectron 86:262-269 |
| abstractText | The accumulation of macrophages (MPhi) at the sensor-tissue interface is thought to be a major player in controlling tissue reactions and sensor performance in vivo. Nevertheless until recently no direct demonstration of the causal relationship between MPhi aggregation and loss of sensor function existed. Using a Continuous Glucose Monitoring (CGM) murine model we previously demonstrated that genetic deficiencies of MPhi or depletion of MPhi decreased MPhi accumulation at sensor implantation sites, which led to significantly enhanced CGM performance, when compared to normal mice. Additional studies in our laboratories have also demonstrated that MPhi can act as "metabolic sinks" by depleting glucose levels at the implanted sensors in vitro and in vivo. In the present study we extended these observations by demonstrating that MPhi chemokine (CCL2) and receptor (CCR2) knockout mice displayed a decrease in inflammation and MPhi recruitment at sensor implantation sites, when compared to normal mice. This decreased MPhi recruitment significantly enhanced CGM performance when compared to control mice. These studies demonstrated the importance of the CCL2 family of chemokines and related receptors in MPhi recruitment and sensor performance and suggest chemokine targets for enhancing CGM in vivo. |
