New protein switch that could stop the progression of blood-poisoning

Little is known regarding the molecular switches and pathways that regulate this disease.

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Sepsis is a life-threatening illness caused by your body’s response to an infection. It develops when the chemicals the immune system releases into the bloodstream to fight an infection cause inflammation throughout the entire body instead.

The illness causes an estimated 14 million deaths every year.

In a new study by the University of British Columbia, scientists have identified a key protein that they think, plays a vital role in regulating the progression of sepsis.

Sepsis occurs in two phases: 1. Systemic inflammatory response syndrome (SIRS) that results in a “cytokine storm,” a dramatic increase in immune cells such as macrophages, a type of white blood cell.

This causes inflammation and a decrease in anti-inflammatory cells and thus leads to chemical imbalances in blood and damage to tissues and organs.

Recovery starts to take place when the body enters a second phase called the endotoxin tolerance (ET) phase, where the opposite occurs.

Scientists examined the role of a protein called ABCF1 in white blood cells during inflammation in a mouse model of sepsis. They discovered that ABCF1 could act as a “switch” in sepsis to transition from the initial SIRS phase into the ET phase and regulate the “cytokine storm.”

They also found that without the ABCF1 switch, immune responses are stalled in the SIRS phase, causing severe tissue damage and death.

Hitesh Arora, co-lead author of the study who conducted this research as a Ph.D. student at the Michael Smith Laboratories at UBC said, “Sepsis triggers an uncontrolled chain-reaction of inflammation in the body, leading to tissue damage, organ failure, and death. We have discovered that the enzyme ABCF1 acts as a ‘switch’ at the molecular level that can stop this inflammatory chain-reaction and dampen the potential damage.”

senior author Wilfred Jefferies, a professor at the Michael Smith Laboratories and departments of medical genetics and microbiology and immunology at UBC said, “Our study may lead to therapies that overcome inflammatory and autoimmune disease such as rheumatoid arthritis, inflammatory bowel disease, Crohn’s disease, and ulcerative colitis. The discovery opens up the potential for new treatments for chronic and acute inflammatory diseases, as well as auto-immune diseases.”

The study was published recently in journal Immunity.