Examining the Regulation of TLR2 in Undifferentiated and Differentiated Neuro2a Cells Following Stimulation with Lipopolysaccharide (LPS)
Loading...
Authors
Annie Singh
Issue Date
2026
Type
Language
Keywords
Alternative Title
Abstract
Inflammation is an essential part of normal immune system functioning and is the mechanism for the body to respond to insult and foreign pathogens. However, chronic inflammation has long been understood to be pathogenic in many disease states, including diabetes mellitus (DM), cardiovascular disease (CVD), stroke, and Alzheimer’s disease (AD). This research aims to explore how inflammatory conditions influence the regulation of Toll-Like Receptor 2 (TLR2), a key receptor involved in innate immune signaling. The current study investigates the regulation of TLR2 in both undifferentiated and differentiated Neuro-2a (N2a) cells in the presence of lipopolysaccharide (LPS). N2a cells are mouse neuroblastoma cells that display characteristics of both neuronal and amoeboid stem cells, having been isolated from fetal mouse brain tissue. Although N2a cells are not immune cells, they respond to inflammatory stimuli, making them valuable for studying neuron-inflammation interactions. LPS, an endotoxin found in bacteria, is frequently used in laboratory settings and serves as a trigger for innate immune responses. Recent studies have shown that neurons can express various members of the TLR family, indicating that immunoreactivity is present in neurons as well. This project consists of four groups. Group 1, a control group, will have N2a cells undifferentiated without LPS, and Group 2 will have N2a cells undifferentiated with LPS. Group 3, a control group, will have N2a cells differentiated using 1% bovine serum albumin (BSA) without LPS, and Group 4 will have N2a cells differentiated using 1% BSA with LPS. We hypothesize that the TLR2 receptor is overexpressed in differentiated N2a cells compared to undifferentiated cells, and that its expression increases further in cells exposed to LPS. These findings will contribute to the understanding of neuron-like cells being capable of detecting and reacting to inflammatory cues.