CD300f · Unravelling the role of the immune receptor CD300f in spinal cord injury and metabolic reprogramming
Horizon 2020 — Marie Skłodowska-Curie Actions
- Duration
- 2021-10-01 → 2023-09-30
- EU contribution
- €172,932
- Participants
- 1
- Scheme
- MSCA-IF
Lines connect the coordinator with its partners.
Results in brief
Unravelling the role of the immune receptor CD300f in spinal cord injury and metabolic reprogramming
Spinal cord injury (SCI) is a leading cause of death and disability in individuals under 40, mainly men. The societal and individual costs of SCI are significant, yet there is currently no effective treatment for humans. SCI induces systemic immune suppression and triggers a local inflammatory response in the injured spinal cord, leading to secondary damage. While inflammation is crucial for homeostasis, the balance between destructive and protective aspects must be precisely regulated for CNS repair and recovery. Recent focus has been on immune receptors as potential targets for controlling microglia/macrophage responses post-SCI. The project aims to assess the role of the CD300f immune receptor and its metabolic reprogramming in neurorestoration after SCI. Additionally, the efficiency of a mitochondrial modulator as a novel neuroprotective strategy is being tested. The study involved inducing spinal cord contusion injury in CD300f knockout mice, evaluating functional outcomes and histopathological parameters.
Data: CORDIS, © European Union
Project objective
Inflammation after spinal cord injury (SCI) exerts a key effect on the progress of both degeneration and regeneration after a traumatic injury. In addition, it has become increasingly clear that understanding the interaction between metabolism and immune function can provide an insight into cellular responses to different challenges. Recent reports from our group and others, suggest that metabolic reprogramming and immune receptors play an orchestrated role in modulating microglia and macrophage phenotype. An interesting example is CD300f, a very unique immune receptor that: i) displays a dual activating/inhibitory capacity; ii) is important for the phagocytosis of apoptotic cells and putatively of synapses; and iii) regulates microglia immunometabolic phenotype. Our hypothesis postulates that, by modulating immunometabolism, CD300f plays an important role in neuroprotection under neuroinflammatory conditions. In the current project, we propose to addresses the interplay between inflammation and metabolic reprogramming by evaluating the role of microglia/macrophage CD300f and their metabolic reprogramming after SCI. We will also test the efficacy of a mitochondrial modulator as a novel neuroprotective strategy for the stimulation of microglial mitochondrial oxidative metabolism.This proposal is based on a set of unpublished data produced by both the ER at the Institut Pasteur Montevideo and the host institution. We will use novel tools generated by our group as the CD300floxP mice, that crossed with CX3CR1-Creert mice will enable to the conditional CD300f KO in microglia and barrier macrophages, and compare these results with global KO mice. The results generated will provide novel insights related to the mechanisms underlying SCI, and for the understanding of how the immune system and the metabolism dialogue in SCI. This could have important implications in a broad spectrum of neurological diseases, where inflammation contribute detrimentally to the pathology.
Original text from CORDIS.
Participants
- UNIVERSITAT AUTONOMA DE BARCELONA · Cerdanyola Del VallesCoordinatorSpain
Links
Data: CORDIS, © European Union