RCSI researchers have discovered a new way to ‘put the brakes’ on excessive inflammation by regulating a type of white blood cell that is critical for our immune system. The discovery has the potential to protect the body from unchecked damage caused by inflammatory diseases, said the researchers. The paper, led by researchers at RCSI University of Medicine and Health Sciences, was published recently in Nature Communications.

When immune cells (white blood cells) in our body called macrophages are exposed to potent infectious agents, powerful inflammatory proteins known as cytokines are produced to fight the invading infection. However, if these cytokine levels get out of control, significant tissue damage can occur.

The researchers have found that a protein called arginase-2 works through the energy source of macrophage cells, known as mitochondria, to limit inflammation. Specifically, they have shown for the first time that arginase-2 is critical for decreasing a potent inflammatory cytokine called IL-1. This discovery could allow researchers to develop new treatments that target the arginase-2 protein and protect the body from unchecked damage caused by inflammatory diseases.

“Excessive inflammation is a prominent feature of many diseases, such as multiple sclerosis, arthritis and inflammatory bowel diseases. Through our discovery, we may be able to develop novel therapeutics for the treatment of inflammatory disease and ultimately improve the quality of life for people with these conditions,” commented senior author on the paper Dr Claire McCoy, Senior Lecturer in Immunology at the RCSI.

The study was led by researchers at the School of Pharmacy and Biomolecular Sciences, RCSI (Dr Claire McCoy, Dr Jennifer Dowling and Ms Remsha Afzal) in collaboration with a network of international researchers from Australia, Germany, and Switzerland. The research was funded by Science Foundation Ireland, with initial stages of the research originating from a grant from the National Health Medical Research Council, Australia.