Deadly Contact: Researchers discover a potential method to combat sepsis.

Researchers from the University of Connecticut School of Medicine have made a significant discovery regarding the deadly progression of sepsis — a condition that, according to the World Health Organization (WHO), claims 11 million lives worldwide each year.

The scientists managed to investigate the lethal process associated with sepsis, bringing them closer to preventing fatal outcomes for affected individuals, as reported by University of Connecticut.

A study published on January 23 in the journal Cell revealed how dying cells inadvertently trigger a fatal chain reaction among neighboring cells, fueling the severe inflammation characteristic of sepsis. Sepsis occurs when the body's immune response to an infection spirals out of control, leading to widespread inflammation, organ failure, and often death.

While it was long believed that infections solely caused this inflammatory response, recent studies indicate that uninfected cells play a crucial role in the process. These healthy cells behave as if they are infected, dying and sending harmful signals to neighboring cells, which contributes to the continuation of the inflammatory cycle.

The University of Connecticut team has now identified these signals as vesicles — tiny membrane-bound bubbles that dying cells release in a desperate attempt to survive. The process begins with genuinely infected cells trying to stop the spread of pathogens. These cells release a protein called gasdermin-D on their surface, which forms pores that puncture the cell membrane, resulting in cell death and the release of its contents.

However, some cells attempt to evade death by expelling portions of their damaged membranes that contain these gasdermin-D pores. The expelled membranes form vesicles that float freely. When these vesicles encounter nearby healthy cells, the gasdermin-D pores integrate into their membranes, sequentially killing them.

This chain reaction of death spreads inflammation and exacerbates the symptoms of sepsis. Vijay Rathinam, an immunologist at the University of Connecticut School of Medicine and lead author of the study, describes this process: "When a dying cell releases these vesicles, they can simply transfer these pores to the surface of a neighboring healthy cell, leading to its death."

This unintended side effect, where cells try to save themselves, contributes to the inflammation observed in sepsis. Currently, Rathinam and his team are exploring ways to suppress the formation or functioning of gasdermin-D vesicles, which could pave the way for new treatments not only for sepsis but also for other inflammatory diseases.

Such research is a crucial step toward understanding the cellular mechanisms that cause dangerous diseases, highlighting the complex interplay between infection, our body, and inflammation. The discovery of gasdermin-D vesicles has opened a new chapter in the fight against inflammatory diseases, offering hope for more effective treatment methods in the future.

Important! This article is based on the latest scientific and medical research and does not contradict them. The text is for informational purposes only and does not contain medical advice. For diagnosis, please consult a doctor.