Related Experiment Video
Updated: Aug 13, 2026
07:08
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Sublethal bisphenol A compromises BV-2 microglial immunity by disrupting TLR4 signaling through the
Ching-Tien Lee1, Cheng-Fang Hsieh2, Jiz-Yuh Wang3
1Department of Nursing, College of Nursing, National Taipei University of Nursing and Health Sciences, Taipei 112303, Taiwan.
Neurotoxicology
|August 11, 2026
Summary
Bisphenol A (BPA) exposure impairs microglial immune responses, suppressing inflammatory signaling and antioxidant pathways. This neurotoxicant disrupts brain innate immunity, potentially increasing neuropathic risk.
Area of Science:
- Neuroscience
- Immunology
- Environmental Health
Background:
- Bisphenol A (BPA) is a widespread environmental contaminant linked to neurotoxicity and neurodegenerative diseases.
- Microglia play a crucial role in brain immune homeostasis, and their dysfunction is implicated in neuropathology.
Purpose of the Study:
- To investigate the impact of sublethal Bisphenol A (BPA) exposure on microglial immune reactivity.
- To elucidate the mechanisms by which BPA interferes with microglial inflammatory and signaling pathways.
Main Methods:
- Utilized an in vitro BV-2 microglial cell model.
- Assessed immunoinflammatory responses following sublethal BPA exposure, with and without lipopolysaccharide (LPS) stimulation.
- Analyzed cytokine secretion, inflammasome activation, antioxidant expression, and key signaling pathway modulation (MAPK, Akt, NF-κB, ROS/Nrf2-Keap1/HO-1, TLR4).
Main Results:
- Sublethal BPA exposure suppressed basal and LPS-induced microglial immune activity without affecting cell viability.
- Observed reduced pro- and anti-inflammatory cytokine secretion and altered NLRP3 inflammasome processing.
- Demonstrated BPA-induced downregulation of MAPK, Akt, and NF-κB pathways, coupled with ROS-dependent upregulation of the Nrf2-Keap1/HO-1 axis, interfering with TLR4 signaling.
Conclusions:
- Sublethal Bisphenol A (BPA) interferes with Toll-like receptor 4 (TLR4)-mediated immunoinflammatory signaling in microglia.
- The observed effects are potentially mediated by modulation of the reactive oxygen species (ROS)/Nrf2-Keap1/heme oxygenase-1 (HO-1) axis.
- Disruption of microglial immune function by BPA highlights a potential risk factor for neuropathies.
Related Concept Videos
01:28Regulation of Bacterial Virulence
Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
01:22Gut-Brain Axis
The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...
01:18Dysbiosis of the Gut Microbiota
The human gut microbiome includes a diverse array of microbial species, including beneficial commensals and opportunistic pathogens, which interact to support host health. These microbes contribute to essential functions such as nutrient metabolism, immune system modulation, and maintenance of intestinal barrier integrity. However, disruptions to this equilibrium—referred to as dysbiosis—can have widespread physiological consequences.Dysbiosis is often characterized by reduced microbial...