Small peptide produced by bowel bacteria recognized as a key factor in kidney fibrosis

A molecule of bacteria in the gut can resurrect a kidney walk, where a chain reaction of inflammation, scars and fibrosis – a serious complication of diabetes and a major cause of renal failure – according to a new study by researchers at the University of Illinois and University of Illinois researchers.

After finding high levels of Corisin – a small peptide produced by Grapefruit The bacteria in the intestine – in the blood of patients with kidney diabetic fibrosis, researchers used computer simulations and tissue and mouse experiments to follow how Corisin affects the kidneys, how it gets there from the gut and a possible treatment method.

“Previous studies have shown us that Conein can damage the cells and worsen the scars and fibrosis of tissues in other organs, so we suspected it could be a hidden kidney fibrosis guide,” said Professor Illinois Animal Sciences University of Mie Dr. Esteban Gabazza. Cann and Gabazza are subsidiaries of the Carl R. Woeese genomic biology Institute in Illinois. “Our new findings suggest that Corisin is indeed a hidden culprit behind progressive kidney damage to diabetes and that blocking could provide a new way of protecting kidney health to patients.”

The researchers published their findings in Nature Communications magazine.

Diabetic kidney fibrosis is an important cause of kidney failure worldwide, but the key factors in her computer science have remained a mystery and no treatments can stop the process, said Dr. Taro Yasuma of Mie University, a physician and the first writer.

Many people with long -term diabetes eventually develop kidney fibrosis and as soon as it proceeds, there are limited options beyond transplantation or kidney transplantation. Current treatments focus mainly on blood sugar control and blood pressure control, but there is no cure that stops or reversing the scars or fibrous process. ”

Dr. Taro Yasuma of Mie University

Researchers began examining blood and urine patients with diabetic kidney disease. They found that the patients had significantly more Korisin than their healthy counterparts and that the amount of blood corisin was associated with the extent of kidney damage.

After seeing the same results in kidney fibrosis mice, the researchers watched what Koristina did in the kidneys of the mice. They found that Korisin accelerates aging in kidney cells, starting with a chain reaction from inflammation to cell death in scarring, eventually leading to loss of kidney function and worsening fibrosis.

But how did Corisin get out of the gut in the kidneys? The Cann and Gabazza teams worked with U. of I. Chemical and Biomolecular Engineering Professor Diwakar Shukla to produce computer simulations and laboratory experiments to follow Corisin’s journey from the intestine to blood circulation. They found that Korisine can adhere to albumin, one of the most common blood proteins, and lead it through blood circulation. When it reaches the kidneys, Corisin disconnects from albumin to attack the subtle structures that filter blood and urine.

To confirm that Corisin was the main culprit behind kidney damage, the researchers gave the mice antibodies against Corisin. Saw a dramatic decrease in kidney speed.

“When we deal with mice with an antibody that neutralizes Korisine, it slows down kidney aging and significantly reduced kidney scars,” said Gabazza, who is also an Assistant Professor of Animal Sciences in Illinois. “While such an antibody for use in humans has not been approved at this time, our findings show that it could develop into a new treatment.”

Researchers then plan to try anti -isisine treatments on more advanced animal models, such as pigs, to explore how they could adapt for safe use to humans. U. Of I. and MI University have a common notification of inventions in Corisin antibodies.

“Our work suggests that the blockage of Koregine, either with antibodies or other targeted treatments, could slow down or prevent kidney scars in diabetes and thus enhance the quality of life of patients,” Cann said.

This study was supported by Japan Science and Technology, the Japanese Society for the Promotion of Science, the Takeda Foundation, The Takeda Science Foundation

The Japanese Union for Diabetes Education and Care, Eli Lilly Japan Innovation Research Grant, the Daiwa Security Foundation and the Charles and Margaret Levin Foundation. Cann is also a Professor of Microbiology and Nutrition Sciences and a member of the East Asian and Pacific studies in Illinois.