New antibody for bowel disease

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UConn molecular and cell biologist Michael Lynes and an international team of researchers have been awarded a patent for a novel antibody that could be proven safe than other drugs currently available.

IBD and current treatments:

More than 1.6 million Americans have IBD. Two of the most common forms of IBD are Crohn’s disease and ulcerative colitis, chronic but treatable conditions that affect children and adults. One in 10 people with IBD are under 18, according to the Crohn’s & Colitis Foundation.

Existing antibody treatments for IBD are ineffective in some patients and also pose risk to the normal functioning immune system.

Study on Metallothionein:

More than a decade ago, Lynes, professor and head of the Department of Molecular and Cell Biology at UConn, and his research team discovered a novel and important role that a protein called metallothionein (MT) plays in influencing the body’s immune function. The body produces MT when cells are under stress, and extended periods of stress cause MT to be released from the cells that produced it, Lynes says. MT is an unusual protein that holds onto chemicals in the body – both those that are beneficial, such as zinc and copper, and those that are harmful – such as cadmium and mercury.

During the study, Lynes and his research team noticed that MT released from cells could mimic some of the signals that the immune system uses as cues to tell cells to go to one place or another in the body. Under normal circumstances, immune cells use these signals to guide them to local infections or other damaged tissues. When these cells are stressed over prolonged periods, this can mean that there is persistent inflammation accompanied by damage to nearby healthy tissue.

Over 80 autoimmune diseases have been identified and are becoming increasingly prevalent. About 20% of the U.S. population suffer from some form of autoimmune disease or chronic inflammation. While the causes remain largely unknown, it is believed that they are probably triggered by a combination of genetic and environmental factors.

Co-study:

A team of Belgium doctors and scientists studying IBD had published a paper saying that their sickest patient’s bodies produced the most MT. This protein serves as a normal part of the cell’s internal machinery inside the cell, gets outside the cell and causes damage.

That paper by Dr. Martine DeVos, Debby Laukens, and Lindsey Devisscher led to a collaboration with Lynes. Since the protein serves an essential purpose, they pondered on ways to stop MT form prolonging inflammation and damaging heathy cells.

New antibody:

Lynes and team produced an antibody that attaches itself to MT, when outside the cells and inactivates it. Thereby it prevents they body from attacking its intestinal system. This approach dramatically reduced IBD in mouse models of the human disease.

“It’s like we have created a partner for MT that binds it and hugs it and won’t let it go,” Lynes says. The UConn team has been testing this treatment on mice and is working on creating a form of antibody that their collaborators can test in humans.

Lynes work is significant because there is a great deal of research being done to try to keep autoimmune diseases at bay, his work seeks to learn more about the causes. Auto Immune diseases are at an increasing trend in both developing and industrialized countries, so his work has strong public health and commercial potential.

Meanwhile, Lynes is also working with Ciencia Inc., an East Hartford-based biotech company, to develop a test that could measure 1,000 different kinds of molecules in a drop of blood to find patterns of molecular biomarkers that can serve as red flags for the early onset of autoimmune disease.

This research has the potential to identify someone’s propensity to develop an autoimmune disease and to enable treatments that are more effective. Often, by the time people have symptoms of autoimmune disease and consult their doctor, irreparable damage has already been done to their bodies. Developing these biomarkers wont cure the disease, however would lead to early intervention minimizing the damage.