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Researchers are discovering new ways to stop inflammation in the lungs due to sepsis and injury

Researchers from the University of Calgary at the Cumming School of Medicine (CSM) under the direction of Drs. Donna Senger, PhD, Paul Kubes and Stephen Robbins, PhD, have found a new way to stop harmful inflammation in the lungs due to sepsis and injury patients. The research involved teams from 10 laboratories, nine at the University of Calgary, with researchers from the Arnie Charbonneau Cancer Institute and the Snyder Institute for Chronic Diseases. "The CIHR Institute for Cancer Research

One in 18 deaths in Canada is associated with sepsis, which occurs when the body fights off serious infections, and the immune system speeds up the delivery of white blood cells to eliminate your immune system and immune system Infections lead to inflammation A problem arises when the white blood cells leave the bloodstream and enter the tissues to clear the inflammation, in some cases they stay white instead of tidying up and moving behind it forming blood cells called internal organs can cause damage to the lungs and lead to death.

Sepsis is not the only disease that causes an unhealthy accumulation of white blood cells in the lungs Inflammation from injury and other illnesses can also cause this harmful reaction Acute lung failure is one of the most common Causes of death in the intensive care in Canada.

The collaboration started about 1

5 years ago. It was a project based on a similar premise and had to solve two different problems. The researchers wanted to know why some cells attach themselves to the lungs. Senger and Robbins are cancer biologists and have studied how cancer metastasizes. They knew that some cancer cells target the lungs and somehow stay there and grow. Many people with cancerous tumors do not die from the primary tumor, but from where the cancer metastasizes. In the meantime, the inflammatory specialist Kubes investigated why white blood cells accumulate in the lungs. In diseases such as sepsis, victims often die from the body's response to the disease rather than sepsis itself.

Together, they began to search for a molecule present in both processes. They targeted the lining of blood vessels in the lungs because they suspected that there would be a signal that would allow cancer cells and white blood cells to stop and collect. It was there that they found a molecule that could bind to white blood cells and help cells move from the bloodstream to the tissues during inflammation. As long as these molecules are present, they bind the white blood cells further.

After the scientists understood how and why the white blood cells penetrated the tissue, they looked for a "cut-off" to keep the molecule from binding with the white blood cells. The teams developed a drug-like molecule that prevents the binding of white blood cells to the molecule when it is introduced into the bloodstream.

"says Kubes, director of the Snyder Institute for Chronic Diseases at the CSM and professor in the Department of Physiology and Pharmacology." It could affect any inflammatory condition in which lung injury contributes to the deterioration of a patient's condition. "

With this knowledge, the researchers have found a similar process in the liver, they have now patented two drug-like molecules that can prevent lung and liver damage due to inflammation." While all of the research that has been done on mice is currently underway Phase I clinical trial to begin with human testing.

Researchers also apply results to cancer metastasis, hoping this new understanding could lead to cancer therapies "The discovered molecule binds both white blood cells and certain cancer cells n, "says Senger, a research associate at the Department of Oncology. "We have developed a method to prevent white blood cells from binding and invading tissue, and now we hope to find a solution to prevent the spread of cancer cells to these organs."


Journal Reference:

Choudhury, SR et al. . (2019) Dipeptidase-1 is an adhesion receptor for the recruitment of neutrophils into the lung and liver. Cell . doi.org/10.1016/j.cell.2019.07.017.[19659016[//
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