| First Author | Duan L | Year | 2018 |
| Journal | Neuron | Volume | 100 |
| Issue | 1 | Pages | 183-200.e8 |
| PubMed ID | 30269986 | Mgi Jnum | J:272730 |
| Mgi Id | MGI:6284929 | Doi | 10.1016/j.neuron.2018.08.030 |
| Citation | Duan L, et al. (2018) PDGFRbeta Cells Rapidly Relay Inflammatory Signal from the Circulatory System to Neurons via Chemokine CCL2. Neuron 100(1):183-200.e8 |
| abstractText | Acute infection, if not kept in check, can lead to systemic inflammatory responses in the brain. Here, we show that within 2 hr of systemic inflammation, PDGFRbeta mural cells of blood vessels rapidly secrete chemokine CCL2, which in turn increases total neuronal excitability by promoting excitatory synaptic transmission in glutamatergic neurons of multiple brain regions. By single-cell RNA sequencing, we identified Col1a1 and Rgs5 subgroups of PDGFRbeta cells as the main source of CCL2. Lipopolysaccharide (LPS)- or Poly(I:C)-treated pericyte culture medium induced similar effects in a CCL2-dependent manner. Importantly, in Pdgfrb-Cre;Ccl2(fl/fl) mice, LPS-induced increase in excitatory synaptic transmission was significantly attenuated. These results demonstrate in vivo that PDGFRbeta cells function as initial sensors of external insults by secreting CCL2, which relays the signal to the central nervous system. Through their gateway position in the brain, PDGFRbeta cells are ideally positioned to respond rapidly to environmental changes and to coordinate responses. |
