Topic: LPS

Prenatal alcohol exposure (PAE) leads to immune system dysfunction and increased susceptibility to autoimmune diseases. To explore potential mechanisms by which PAE induces neuroimmune dysfunction, the current study examined the impact of PAE on toll-like receptor 4 (TLR4) and TLR7/8 activation. Pregnant rats were divided into two groups: PAE - liquid ethanol diet ad libitum, and CON - pelleted control diet ad libitum. Male and female offspring were challenged in adulthood with LPS (40 µg/kg; activates TLR4), R848 (1 mg/kg; activates TLR7/8), or DMSO (vehicle), followed by brain sample collect

Maternal infections and prenatal inflammation are recognized risk factors for neurodevelopmental diseases. Astrocytes are glial cells essential for synapse formation and refinement, but they also may react to inflammatory environment affecting neuronal network homeostasis. However, how an inflammatory episode occurring during fetal development influences astrocyte generation and phenotype remains largely unknown.In the brain, the innate immune molecule Pentraxin3 (PTX3) is produced by astrocytes and promotes the maturation of excitatory synapses. Its expression is induced by inflammatory stimu

Parkinson’s disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Among other factors, microglia are thought to take part in the chronic neuroinflammatory scenario that contributes to the process of neuronal death. However, the factors that maintain the overreactive response of microglia in PD remain mysterious. As we wanted to simulate the chronic neuroinflammatory scenario taking place in PD, we evaluated the response of microglial cells after repetitive pro-inflammatory stimuli induced by LPS and IFN-g in vitro. In contrast w

The transcription factor Nrf2 (encoded by the Nfe2l2 gene) is a widely-expressed stress-responsive master regulator of several aspects of homeostatic physiology. Nrf2 plays a key role in preventing oxidative stress and inflammation. In the brain, Nrf2 is highly expressed by endothelial cells. Brain endothelial cells (BECs) are the key component of the blood brain barrier (BBB), which controls brain homeostasis. The role of BEC Nrf2 expression in maintaining homeostasis is not fully understood. In this project, through gain- and loss function experiments, we have found that Nrf2 activity in BEC

Neuroinflammation represents a physiological response marked by immune cell activation and the release of inflammatory markers within the central nervous system. While it plays a pivotal protective role, when dysregulated it is also implicated in various neurological disorders such as Alzheimer disease. Brain organoids, self-organized three-dimensional (3D) aggregates derived from human induced pluripotent stem cells (iPSC), have emerged as a novel model to study brain development and disease. This study focuses on the development of a cerebral organoid model of neuroinflammation using pro and