Publications by authors named "Conceicao E Anibal Silva"

Psoriasis is a chronic and recurrent inflammatory skin disease characterized by abnormal proliferation and differentiation of keratinocytes and activation of immune cells. However, the molecular driver that triggers this immune response in psoriatic skin remains unclear. The inflammation-related gene absent in melanoma 2 (AIM2) was identified as a susceptibility gene/locus associated with psoriasis.

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Background: Neuroinflammation in Alzheimer's disease (AD) can occur due to excessive activation of microglia in response to the accumulation of amyloid-β peptide (Aβ). Previously, we demonstrated an increased expression of this peptide in the locus coeruleus (LC) in a sporadic model for AD (streptozotocin, STZ; 2 mg/kg, ICV). We hypothesized that the STZ-AD model exhibits neuroinflammation, and treatment with an inhibitor of microglia (minocycline) can reverse the cognitive, respiratory, sleep, and molecular disorders of this model.

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  • Resident macrophages, specifically sNAMs in sensory ganglia, adapt to various tissue environments and are involved in physiological functions as well as pain conditions like neuropathic pain.
  • Following peripheral nerve injury, there's an increase in macrophage numbers in the sensory ganglia, which is debated to be due to local resident cell growth or blood monocyte infiltration.
  • Studies confirm that the rise in macrophages after nerve injury is due to the proliferation of resident CX3CR1 macrophages, which produce pro-inflammatory cytokines and contribute to neuropathic pain development.
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  • Zika virus (ZIKV) can cause significant neuronal cell death by damaging cells and activating apoptotic pathways, but the role of reactive oxygen species (ROS) in this process is unclear.
  • This study focused on human neuroblastoma cells (SH-SY5Y) and examined how ZIKV infection affects cell survival and the expression of genes related to cell death.
  • Results showed that while ZIKV infection led to high cell death and changes in gene expression, the levels of ROS did not increase, and using a ROS scavenger had no effect on preventing cell death, indicating that ROS is not the main cause of cell death in this context.
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Zika virus (ZIKV) infection during pregnancy is associated with microcephaly, a congenital malformation resulting from neuroinflammation and direct effects of virus replication on the developing central nervous system (CNS). However, the exact changes in the affected CNS remain unknown. Here, we show by transcriptome analysis (at 48 h post-infection) and multiplex immune profiling that human induced-neuroprogenitor stem cells (hiNPCs) respond to ZIKV infection with a strong induction of type-I interferons (IFNs) and several type-I IFNs stimulated genes (ISGs), notably cytokines and the pro-apoptotic chemokines CXCL9 and CXCL10.

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