Duke scientists found that exercise can really prevent being "bullyed" by inflammation!

In a new study published in Science Advances, a team of researchers from Duke University in the United States demonstrated that the body's muscles themselves have a natural ability to resist the devastating effects of chronic inflammation while moving.
inflammation itself is not good or bad.
when the body is injured, the initial low-level inflammatory response removes cell fragments and helps the tissue rebuild.
but when the immune system overreacts, it produces inflammatory reactions that cause damage, such as deadly cytokine storms in some patients with neocyto pneumonia.
addition, there are diseases that can lead to chronic inflammation, such as rheumatoid arthritis and myocardial dystrophy, which can lead to muscle atrophy and weaken their ability to contract.
healthy skeletal muscles have a strong regenerative capacity to respond to minor injuries by activating, multiplying and differentiating muscle stem cells, a process that contributes significantly to local and systemic inflammatory responses.
, in particular interferon γ (IFN-γ), an important anti-inflammatory cytokine, has been shown to be associated with various types of muscle atrophy and dysfunction.
Though previous studies in humans and animals have shown that exercise can generally help mitigate the effects of inflammation, it is difficult to distinguish between what role muscle cells themselves play in it and how they interact with specific disease-caused molecules such as interferon-γ.
, author of the study and a professor in the Department of Biomedical Engineering at Duke University, said: "There are many biological processes in the body during exercise, but it is difficult to distinguish which systems and cells do in the moving human body.
we have built an engineering muscle platform and it is modular, which means we can mix and match all types of cell and tissue components on demand.
, we found that muscle cells were able to act as anti-inflammatory on their own.
to demonstrate the destructive power of muscles to stop interferon γ, the team turned to an engineering muscle platform that their lab has been developing for nearly a decade.
previously, they had developed contracting and functioning human skeletal muscles in a petri dish, and since then the lab has been improving its process by adding immunocellular and stem cell libraries to the formula.
the new study, researchers soaked these fully functional engineered muscles in relatively high levels of interferon γ for seven days to simulate the effects of chronic inflammation over a long period of time.
as expected, the muscles become smaller and lose most of their strength.
then, the researchers used interferon γ again, but this time by stimulating muscles with a pair of electrodes to simulate the effects of exercise, a process they hope will induce some muscle growth.
, they were surprised to find that engineered human muscles almost completely blocked the effects of chronic inflammation.
it inhibits a specific molecular pathway in myoblasts, and the two drugs used to treat rheumatoid arthritis, tofatinib and ballitinib, block exactly the same anti-inflammatory pathway. "Our study not only confirms that interferon γ works primarily through a specific signaling pathway, but also suggests that moving muscle cells can directly fight this inflammatory signal without relying on other cell types or tissues," said Zhaowei Chen, lead author of the
study and a postdoctoral researcher at Bursac Labs.
, Bursac said, "When moving, muscle cells directly fight anti-inflammatory signals induced by interferon γ, which we didn't expect."
results show that engineered muscles are valuable in discovering new mechanisms and potential treatments for disease.
there is a view that the best levels and methods of exercise can combat chronic inflammation without excessive pressure on cells.
perhaps through our engineered muscles, we can help verify that this view is correct.
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