We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Microplastics induced inflammation in the spleen of developmental Japanese quail (Coturnix japonica) via ROS-mediated p38 MAPK and TNF signaling pathway activation1
Summary
Young Japanese quail fed polystyrene microplastics at environmentally relevant doses developed significant inflammation in their spleens, a key immune organ. The microplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to tissue damage and immune dysfunction. This study adds to evidence that microplastic exposure can harm the immune system in birds, with potential implications for wildlife health and, through the food chain, for humans who consume poultry.
Microplastics (MPs) have been found in virtually every environment on earth and become a source of pollution around the world. The toxicology of microplastics on immunity is an emerging area of research, and more studies are needed to fully understand the effects of microplastics exposure on animal health. Therefore, we tried to determine the immunotoxic effects of microplastics on avian spleen by using an animal model- Japanese quail (Coturnix japonica). One-week chicks were exposed to environmentally relevant concentrations of 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastics in the feed for 5 weeks. The results demonstrated that microplastics induced microstructural injuries featured by cell disarrangement and vacuolation indicating splenic inflammation. Ultrastructural damages including membrane lysis and mitochondrial vacuolation also suggested inflammatory responses in the spleen by microplastics exposure. Meanwhile, increasing reactive oxygen species (ROS) and Malondialdehyde (MDA) while the inactivation of superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) indicated oxidative stress in the spleen. Moreover, the increasing level of proinflammatory cytokines including Tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin-1β (IL-1β), interleukin-6 (IL-6) and decreasing level of anti-inflammatory cytokine interleukin-10 (IL-10) implied splenic inflammation. Furthermore, transcriptomic analysis showed that microplastics induced inflammatory responses in the spleen through p38 mitogen-activated protein kinases (p38 MAPK) pathway activation and tumor necrosis factor (TNF) signaling stimulation. The signaling stimulation also aggravated cell apoptosis in the spleen. The present study may benefit to understand potential mechanisms of developmental immunotoxicology of microplastics.
Sign in to start a discussion.
More Papers Like This
Toxicity induced via ingestion of naturally-aged polystyrene microplastics by a small-sized terrestrial bird and its potential role as vectors for the dispersion of these pollutants
Researchers exposed Japanese quail to naturally aged polystyrene microplastics to evaluate health effects from ingestion. The study found significant body weight reduction, increased oxidative damage in the liver, brain, intestine, and gizzard, and evidence that birds can transport microplastics to new environments through excretion. These findings suggest that even small terrestrial birds may serve as vectors for microplastic dispersal.
The effects of microplastics exposure on quail's hypothalamus: Neurotransmission disturbance, cytokine imbalance and ROS/TGF-β/Akt/FoxO3a signaling disruption
Japanese quail exposed to polystyrene microplastics for five weeks showed significant brain damage in the hypothalamus, including structural changes to neurons, disrupted chemical signaling, and inflammation. The microplastics caused oxidative stress and interfered with important cell-survival pathways in the brain. While studied in birds, these neurotoxic effects are relevant because similar brain pathways exist in humans, and they suggest microplastic exposure could affect neurological function.
Polystyrene microplastics mediate inflammatory responses in the chicken thymus by Nrf2/NF-κB pathway and trigger autophagy and apoptosis
Researchers exposed chickens to polystyrene microplastics and found significant damage to the thymus, a key immune organ. The microplastics triggered oxidative stress, inflammation, and cell death through specific molecular pathways. The study suggests that microplastic exposure could compromise immune function in animals by damaging organs responsible for immune cell development.
Transcriptomic and metabolomic analysis reveals hepatic lipid metabolism disruption in Japanese quail under polystyrene microplastics exposure
Researchers fed Japanese quail polystyrene microplastics at environmentally relevant concentrations for 35 days and analyzed liver effects using transcriptomics and metabolomics. Low doses caused increased food intake and weight gain with liver lipid accumulation, while high doses led to decreased intake and weight loss, suggesting a hormetic dose-response pattern. The study found that microplastic exposure disrupted hepatic lipid metabolism pathways and caused liver oxidative stress in birds.
New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.