We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene microplastics induce kidney injury via gut barrier dysfunction and C5a/C5aR pathway activation
AI summary Read the abstract
In a mouse study, polystyrene microplastics caused kidney damage by first breaking down the gut barrier, which then triggered an immune response that attacked the kidneys through a specific pathway called C5a/C5aR. When researchers repaired the gut barrier or blocked this immune pathway, the kidney damage was prevented. This study reveals a gut-kidney connection that could explain how swallowing microplastics might lead to kidney problems in humans.
Microplastic is an emerging environmental pollutant with potential health risks. Recent studies have shown that microplastic could impair gut homeostasis in mammals. Although it has been widely demonstrated that gut dyshomeostasis could impact renal health through the gut-kidney axis, the effects of microplastic-induced gut dyshomeostasis on renal health and underlying mechanisms are still largely unknown. In the current work, we found that polystyrene microplastics (PS-MPs) treatment impaired the gut barrier, increased urinary complement-activated product C5a levels and renal C5aR expression, leading to chronic kidney disease-related symptoms in mice. Restoring the gut barrier using an antibiotic mixture effectively alleviated PS-MPs-induced kidney injury, indicating the involvement of the gut-kidney axis in PS-MPs-induced renal injury. Moreover, it also mitigated PS-MPs-induced alterations in urinary C5a levels and renal C5aR expression, suggesting that the renal C5a/C5aR pathway might be involved in PS-MPs' impacts on the gut-kidney axis. Further experiments using a C5aR inhibitor, PMX53, verified the vital role of renal C5a/C5aR pathway activation in the development of kidney injury induced by PS-MPs. Collectively, our results suggest that PS-MPs induce kidney injury in mice by impairing the gut barrier, increasing C5a levels, and ultimately activating the renal C5a/C5aR pathway, highlighting the crucial role of the gut-kidney axis in PS-MPs-induced kidney injury.
More Papers Like This
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
AI summary Read the abstract
In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
Toxicological effects of microplastics in renal ischemia–reperfusion injury
AI summary Read the abstract
Researchers studied how microplastic exposure affects kidney injury and recovery in a mouse model of reduced blood flow to the kidneys. They found that microplastics worsened kidney damage by triggering inflammatory responses and disrupting cellular repair processes. The study suggests that microplastic accumulation in the body may increase vulnerability to kidney complications.
Gut and Glomerular Barriers Determine Nanoplastic Fate and Systemic Impact
AI summary Read the abstract
This multi-species study tracked 50 nm polystyrene nanoplastics through zebrafish, isolated mouse kidneys, and cell cultures, finding that nanoplastics are efficiently absorbed through the gut and spread throughout the body but are blocked from accumulating in kidneys by the glomerular filtration barrier. When that barrier was experimentally damaged — mimicking kidney disease — nanoplastics accumulated substantially in the kidneys. This is important because people with kidney disease may face amplified risk from nanoplastic exposure, and gut absorption drives microbiome disruption and systemic inflammation even in healthy individuals.
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
AI summary Read the abstract
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Gut and Glomerular Barriers Determine Nanoplastic Fate and Systemic Impact
AI summary Read the abstract
Tiny plastic particles (like those from breaking-down plastic waste) can easily pass through your gut lining, disrupt your gut bacteria, and trigger inflammation throughout the body, according to a study in zebrafish and mice. The good news: healthy kidneys have a protective filter that normally keeps these nanoplastics from building up—but if that filter gets damaged, plastic particles can accumulate there instead, suggesting that gut health and kidney health may be more connected to plastic exposure than previously thought.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.