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61,005 resultsShowing papers similar to Polystyrene microplastics mediate inflammatory responses in the chicken thymus by Nrf2/NF-κB pathway and trigger autophagy and apoptosis
ClearPolystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
Researchers found that polystyrene microplastics caused testicular damage in chickens through crosstalk between inflammatory and antioxidant defense pathways. Exposure to microplastics through drinking water disrupted the blood-testis barrier, triggered oxidative stress by inhibiting the Nrf2 pathway, activated inflammatory signaling through NF-kB, and ultimately induced cell death in testicular tissue.
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens
Researchers exposed chickens to polystyrene microplastics for 42 days and found significant lung damage, including tissue inflammation and cell stress responses. The microplastics triggered a chain reaction starting with stress in the endoplasmic reticulum (a cell structure involved in protein processing) that activated inflammatory pathways. While this study focused on poultry, similar inflammatory mechanisms could be relevant to understanding how microplastics affect lungs in other species, including humans.
Microplastics induced inflammation in the spleen of developmental Japanese quail (Coturnix japonica) via ROS-mediated p38 MAPK and TNF signaling pathway activation1
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.
Cellular response of THP-1 macrophages to polystyrene microplastics exposure
Researchers exposed human macrophage cells to polystyrene nanoparticles smaller than 450 nanometers and observed significant decreases in cell viability, increased oxidative stress, and DNA damage. The particles also reduced mitochondrial membrane potential and inhibited cell proliferation. The findings suggest that microplastic exposure may impair immune cell function in humans, highlighting potential risks to the immune system.
Toxicological profiling of polystyrene microplastics in raw 264.7 macrophages: Linking microplastic exposure to immune cell impairment
Researchers exposed immune cells called macrophages to polystyrene microplastics and found that the cells rapidly absorbed the particles within two hours. Higher concentrations caused mitochondrial damage, disrupted cellular recycling processes, and triggered inflammation-related signaling. The study provides evidence that microplastics can impair the function of key immune cells responsible for defending the body against foreign threats.
Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Polystyrene microplastics induced oxidative stress, inflammation and necroptosis via NF-κB and RIP1/RIP3/MLKL pathway in chicken kidney
Researchers exposed chickens to different doses of polystyrene microplastics for six weeks to study kidney damage. The study found that microplastic exposure triggered oxidative stress, inflammation, and a form of cell death called necroptosis in kidney tissue through the NF-kappaB and RIP1/RIP3/MLKL signaling pathways.
Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway
After mice inhaled polystyrene microplastics, the particles spread to the brain, liver, kidneys, spleen, and other organs within days, triggering widespread inflammation through a specific immune signaling pathway called TLR/NF-kB. These findings suggest that breathing in microplastics could cause inflammatory damage across multiple organ systems in the body.
The impact of polystyrene nanoplastics on the chicken gut and liver: Based on transcriptomics and microbiomics
Researchers fed polystyrene nanoplastics to chickens for 21 days and found that the particles triggered inflammation and oxidative stress in the gut and liver, damaged the intestinal lining, and disrupted the gut microbiome — with some effects persisting even after exposure stopped. Because poultry is a major protein source for humans globally, these findings raise concerns about nanoplastic contamination in the food supply.
Immunomodulatory and biochemical alterations in chick embryos exposed to polystyrene microplastics
Chick embryos were exposed to polystyrene microplastics at 150 and 300 ug/ml to assess effects on immune system function and key biochemical markers over an incubation period. The study documented immunomodulatory changes and biochemical alterations, raising concerns about developmental effects of microplastic exposure in avian models.
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.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota
Rats exposed to polystyrene microplastics for 90 days developed significant colon inflammation, including damaged gut lining, increased inflammatory markers, and disrupted gut bacteria. The study identified a specific inflammatory pathway (TLR4/NF-kB/COX-2) through which microplastics trigger intestinal inflammation, providing important clues about how plastic particles in food and water could contribute to gut diseases in humans.
Potential toxicity of polystyrene microplastic particles
Researchers investigated the cellular-level toxicity of polystyrene microplastic particles and found that they stimulated immune responses in a size- and concentration-dependent manner. The particles triggered the production of cytokines and chemokines, which are signaling molecules involved in inflammation. The study challenges the common assumption that microplastics pose minimal risk to human health, suggesting they may have immunological effects upon direct contact with cells.
Polystyrene microplastics exacerbate mitophagy through mitochondrial dysfunction in the duck lung
Ducks fed polystyrene microplastics developed lung inflammation and damage through a process where the plastics disrupted the energy-producing mitochondria in lung cells, triggering excessive cell self-destruction. The study confirmed these findings in both live ducks and lab-grown lung cells, showing that the microplastics activated inflammatory pathways and disrupted normal energy metabolism. Since ducks are widely consumed as food, the research highlights how microplastics can damage poultry lung health and provides insights into how inhaled or ingested microplastics might similarly harm human lungs.
Mechanisms underlying mitochondrial dysfunction and intestinal damage induced by ingestion of microplastics in Leuciscus waleckii: The role of the NF-κB/Nrf2 signaling pathway
This study found that polystyrene microplastics harmed juvenile fish by triggering immune dysfunction, oxidative stress, and mitochondrial damage in their intestines. The microplastics activated inflammatory pathways, damaged the intestinal barrier, and shifted the gut microbiome toward harmful bacteria. These findings suggest that microplastic ingestion could have cascading effects on fish health through multiple biological pathways.
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.
Size- and oxidative potential-dependent toxicity of environmentally relevant expanded polystyrene styrofoam microplastics to macrophages
Researchers tested how Styrofoam microplastics of different sizes and weathering conditions affect human immune cells and found that smaller particles, UV-weathered particles, and those from real-world sources were all more toxic. The microplastics triggered inflammation through a pathway called the NLRP3 inflammasome, which is linked to many chronic diseases. This is concerning because most Styrofoam in the environment has been weathered by sunlight, meaning the real-world health risks may be worse than lab studies using fresh materials suggest.
Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp
Researchers exposed carp to polystyrene microplastics and found they caused heart tissue inflammation, cell death, and necrosis through activation of the TLR4/NF-kB inflammatory pathway. The damage increased with higher microplastic concentrations, with both apoptosis and necrosis observed in heart muscle cells. The study provides evidence that microplastic exposure can directly harm cardiovascular tissue in fish.
The crosstalk between M1 macrophage polarization and energy metabolism disorder contributes to polystyrene nanoplastics-triggered testicular inflammation
Researchers investigated how polystyrene nanoplastics cause testicular inflammation in mice by studying the interplay between immune cell behavior and energy metabolism. They found that nanoplastics triggered a pro-inflammatory immune response involving M1 macrophage activation, disrupted cellular energy processes, and caused testicular tissue damage. The study reveals a specific biological mechanism by which nanoplastic exposure may impair male reproductive health.
Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
Researchers investigated the effects of polystyrene nanoplastics on immune cell metabolism and found that macrophages exposed to nanoplastics transformed into lipid-laden foam cells. The study suggests that nanoplastic exposure dysregulates lipid metabolism in immune cells, with implications for understanding how these particles may interact with the immune system at the cellular level.
The effects of nanoplastics on adipose stromal cells from swine tissues
Researchers assessed the effects of polystyrene nanoplastics on adipose stromal cells from pig tissue, finding reduced cell viability after prolonged exposure, increased inflammatory marker TNF-alpha, and elevated oxidative stress markers. These results suggest nanoplastics can disrupt cellular redox homeostasis in adipose tissue at environmentally relevant conditions.