Microplastics clog liver immune cells, driving fat buildup in mice

by Johannes Seiler, University of Bonn

edited by Lisa Lock, reviewed by Robert Egan

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Microplastics appear capable of significantly impairing the function of phagocytes in the liver, at least in mice. In turn, this disrupts the metabolism of this vital organ and increases the build-up of fat inside it. These key findings from a joint German-Austrian study led by the University of Bonn, have now been published in the journal Nature Metabolism.

Phagocytes, literally "eating cells," or "macrophages" to give them their scientific name, are immune cells that reside in virtually every organ of the body. They play an important protective role, looking out for bacteria, diseased cells and foreign matter, engulfing them and breaking them down into their component parts. In addition, they help the organs they live in function properly.

"From working with cell cultures, we've known for several years that macrophages also take up microplastics," explains Professor Elvira Mass from the LIMES Institute at the University of Bonn. "We wanted to know whether that's also the case in a living organism and, if so, what effect it has."

To find out, Mass joined forces with other research groups from the University of Bonn and the University Hospital Bonn (UKB) to focus on a group of macrophages known as Kupffer cells. These reside in the sinusoids, the smallest blood vessels of the liver, where they monitor blood arriving from the gut. Plastic particles that humans or animals swallow and that enter the bloodstream via the gut therefore have to pass by them.

We may ingest up to a credit card's worth of plastic every week

That could mean a lot of particles: Experts estimate that adults ingest up to 5 grams (0.18 ounces) of plastic a week, about the weight of a credit card. With young mice tipping the scales at a mere 20 grams (0.7 ounces), the researchers scaled down the dose accordingly. The individual particles were about the same diameter as an average bacterium.

"We administered microplastics to the animals orally once a week," says Mass, who is also a speaker for the Life and Health Transdisciplinary Research Area (TRA) and a member of the steering committee for the ImmunoSensation3 Cluster of Excellence.

Twelve weeks later, the researchers examined the animals. "We were able to show that the Kupffer cells had taken up large amounts of microplastics," explains Dr. Nikola Makdissi, who ran many of the experiments with his colleague Dr. Maria Francesca Viola.

Macrophages usually digest what they engulf and recycle its component parts. Plastic, however, cannot be broken down and instead clogs the macrophages' "stomachs," the so-called lysosomes. "On the one hand, this means they can no longer take up pathogens or defective cells," Makdissi explains. "On the other hand, they lack important building blocks that they need for their metabolism."

Microplastics clog the macrophages' 'stomachs'

The macrophages react by producing more apolipoproteins, proteins that normally help transport fats in the body. Here, they act as a kind of molecular stress signal. "The surrounding liver cells detect this signal and respond by storing more fat," Mass says. In other words, the disruption to the macrophages' function leads to a metabolic imbalance in the liver.

Plastic particles that are a similar size to bacteria appear to be particularly harmful to the liver. When the researchers instead gave the mice particles that were 10 times smaller, they observed different effects: The "clogging" of the macrophages was much less pronounced, and liver metabolism remained largely unchanged. Instead, the plastic nanoparticles accumulated in the brown adipose tissue (brown fat). Unlike its white counterpart, brown adipose tissue does not primarily store fat but "burns" it to generate heat.

In the mice, the nanoplastics activated the brown adipose tissue and stimulated this heat production. The researchers now want to investigate this effect in more detail.

Publication details

Nikola Makdissi et al, Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism, Nature Metabolism (2026). DOI: 10.1038/s42255-026-01615-8

Journal information: Nature Metabolism

Key medical concepts

MicroplasticsKupffer CellsLysosomes

Clinical categories

GastroenterologyAllergy and immunology Provided by University of Bonn Who's behind this story?

Lisa Lock

BA art history, MA material culture. Former museum editor, paramedic, and transplant coordinator. Editing for Science X since 2021. Full profile →

Robert Egan

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