Mouse study shows microplastics infiltrate blood brain barrier

Much of the millions of metric tons of plastic waste that washes into the sea each year is broken down into tiny fragments by the forces of the ocean, and researchers are beginning to piece together what this means for organisms that consume them. Scientists in Korea have turned their attention toward the top of the food chain by exploring the threat these particles pose to mammal brains, where they were found to act as toxic substances.

In recent years, studies have revealed the kind of threat microplastics pose to marine creatures. This has included weakening the adhesive abilities of muscles, impairing the cognitive ability of hermit crabs and causing aneurysms and reproductive changes in fish. They've turned up in the guts of sea turtles all over the world, and been discovered in seal poo as evidence of them traveling up the food chain. Research has also shown they can alter the shape of human lung cells.

To further our understanding of these dangers, researchers at Daegu Gyeongbuk Institute of Science and Technology orally administered polystyrene microplastics two micrometers in size or smaller to mice over the course of seven days. Like humans, mice have a blood-brain barrier that prevents most foreign substances, and especially solids, from entering the organ, but the scientists found that the microplastics were able to make their way through.

Once in the brain, the scientists found that the particles built up in the microglial cells, which are key to healthy maintenance of the central nervous system, and this had a significant impact on their ability to proliferate. This was because the microglial cells saw the plastic particles as threat, causing changes in their morphology and ultimately leading to apoptosis, or programmed cell death.

Additionally, the scientists carried out experiments on human microglial cells and also observed changes in their morphology, along with changes to the immune system via alterations to the expression of relevant genes, related antibodies and microRNAs. As seen in the mouse brains, this also induced signs of apoptosis.

“The study shows that microplastics, especially microplastics with the size of 2 micrometers or less, start to be deposited in the brain even after short-term ingestion within seven days, resulting in apoptosis, and alterations in immune responses, and inflammatory responses," says study author Dr. Seong-Kyoon Choi." Based on the findings of this research, we plan to conduct additional research that can further reveal the brain accumulation of microplastics and the mechanism of neurotoxicity."

The research was published in the journal Science of The Total Environment. 

 

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New treatment strategy may thwart deadly brain tumours

New research in mice led by investigators at Massachusetts General Hospital (MGH) and the University of Florida reveals a promising strategy that makes glioblastoma susceptible to these medications. The findings, which are published in the Proceedings of the National Academy of Sciences, indicate that such combination therapy should be tested in clinical trials of patients with glioblastoma, for whom there is no known cure.

Part of the reason glioblastoma do not respond well to immune checkpoint inhibitors and other immunotherapies is because cells called myeloid-derived suppressor cells (MDSCs) infiltrate the region surrounding glioblastoma tumours, where they contribute to immunosuppression, tumour progression, and treatment resistance. Thus, targeting these cells may augment immunotherapy and improve responses to treatment in affected patients.

A collaborative effort co-led by Jeffrey K. Harrison, PhD, of the Department of Pharmacology and Therapeutics at the University of Florida, and Rakesh K. Jain, PhD, of the Department of Radiation Oncology at MGH and Harvard Medical School, set out to test this strategy.

Using two mouse models of glioblastoma, the team targeted receptors–called chemokine receptors–that are important for allowing MDSCs to infiltrate into the region surrounding glioblastoma tumours. In mice that were bred to lack chemokine receptor 2 (CCR2) and to develop glioblastoma, MDSCs could not carry out such infiltration.

Treating these mice with an immune checkpoint inhibitor stimulated a strong anti-cancer immune response and prolonged the animals’ survival. In mice with normal CCR2, treatment with a molecule that blocks CCR2 had similar effects.

According to Jain, “The CCR2 antagonist used in this study–called CCX872– has passed phase Ib safety trials in patients with pancreatic tumours, and clinical trials are ongoing to investigate the use of CCR2 inhibitors in several cancers.”

“Thus, the results of this study support targeting CCR2-expressing MDSCs as a means to enhance immunotherapies, and warrant investigation of this combination therapy in clinical trials for patients with glioblastoma,” says Jain.

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