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Browsing ESS - APCT - Posters apresentados em eventos científicos by Author "Bonifácio Andrade, Elva"
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- Regulation of CD47 expression by interferon-gamma under chronic Methamphetamine exposure TitlePublication . Rodrigues, João; Bravo, Joana; Bonifácio Andrade, Elva; Canedo, Teresa; Azevedo, Maria; Summavielle, TeresaExposure to methamphetamine (Meth), a highly addictive widely used psychostimulant, is classically associated with damage to neuronal terminals, but its neurotoxicity can also be mediated via activation of the neuroinflammatory response. Microglia, the resident immune cells of the brain, become highly activated and increase the release of proinflammatory mediators upon exposure to Meth. However, their role in Meth-associated neurotoxicity is still not sufficiently understood. Data from our lab shows that, in the hippocampus, chronic Meth administration leads to microglia homeostasis dysregulation, synapse dysregulation, and downregulation of cluster-differentiation 47 protein (CD47). The crosstalk between CD47 and its receptor, signal regulatory protein α (SIRPα), is an important “don’t eat me signal” that inhibits phagocytosis. CD47 has been shown to protect synapses from excessive microglia-mediated pruning during development and neurodegeneration. Of note, in cancer cells CD47 expression is modulated by interferon-gamma (IFN-γ). Consistently, after chronic Meth, we observed a significant decrease of meningeal T cells, and a decrease in the production of IFN-y by these cells. Here we aim to clarify if IFNγ is regulating CD47 in the brain after chronic Meth administration, and consequently regulating synaptic pruning, using IFNyKO mice and wild-type mice injected with recombinant IFNy via stereotaxic surgery. Preliminary results indicate that IFNy/CD47 does not modulate microglia morphology and number after chronic Meth in the hippocampus. Currently we are evaluating synapses and phagocytosis, and we further expect to clarify the impact of IFNγ /CD47 in the chronic Meth conditioning and in memory.
- Uncovering the microglia response during neonatal Group B Streptococcus meningitisPublication . Soares, Joana; Lorga, Inês; Bravo, Joana; Summavielle, Teresa; Nova, Manuel Vila; Bonifácio Andrade, ElvaGroup B Streptococcus (GBS) remains the most common bacterial cause of meningitis in neonates. Microglia, the brain resident immune cells, have a critical role in the development of neural circuits. However, the role of GBS infection on microglia activation and neurological sequelae remains poorly characterised. Here, we aimed to evaluate whether GBS induces changes in microglia profile during the acute phase of infection, using a mouse model that mimics key steps of GBS pathophysiology in humans. Female C57BL/6 mice were intra-vaginally inoculated with GBS during gestation, and CFU analysis was performed on postnatal days (P) 1, 3 and 5. Bacterial colonisation was found at all ages, peaking at P3. When analysing the status of microglia by flow cytometry in the whole brain of male pups at P3, an overall activation was observed in the infected group. Mainly, we found a significant increase in microglia frequency, as well as the mean fluorescence intensities (MFIs) of CD45, CD11b and F4/80. Additionally, we also analysed some microglial receptors that are important neuro-immune regulators with relevant functions during development. We observed increased CX3CR1 expression in microglia, whereas Sirp and CD200r were not altered. Moreover, analysing the cortex and hippocampus, relevant regions for cognition, we found similar numbers in Iba1+ cells, a known microglia marker, in the hippocampus of infected pups. In contrast, a significant decrease was observed in the cortex, suggesting altered migration of these cells. Furthermore, microglia phagocytosis was increased in the cortex of infected pups but not in the hippocampus. Interestingly, quantification of neurons revealed a significant decrease in the hippocampus of infected pups while being increased in the cortex, compared with age-match controls. Altogether, our results show that GBS meningitis alters the neonatal microglia profile. Further studies will be necessary to better understand the microglia inflammatory state after GBS infection.