The Price of Prosperity: What Would Americans Sacrifice to Preserve Trump’s Tax Cuts?

Americans love Trump's tax cuts. What would they give up to keep them? Most Americans like the Trump tax cuts. Now, Congress must decide what taxpayers would give up in order to keep them.  President Donald Trump mandated sweeping tax relief, especially for corporations and the rich, with his Tax Cuts and Jobs Act of
HomeHealthThe Silent Killer: Understanding Sepsis and Its Devastating Impact

The Silent Killer: Understanding Sepsis and Its Devastating Impact

Like a poison pen, dying cells prick their neighbors with a lethal message. This may worsen sepsis. New findings could lead to a new understanding of this dangerous illness.

Dying cells communicate a deadly signal to their neighboring cells, which might exacerbate sepsis, as reported by Vijay Rathinam and his team from UConn School of Medicine in the January 23 edition of Cell. Their discoveries could pave the way for a better understanding of this serious condition.

According to the World Health Organization (WHO), sepsis is one of the leading causes of mortality globally, claiming around 11 million lives each year. This condition is characterized by unchecked inflammation, typically triggered by an infection. Without prompt and effective treatment, it can result in shock, multiple organ failures, and even death.

Recent research indicates that the root cause of this overwhelming inflammation isn’t solely the infection itself, but rather the cells that become involved. These cells, even in the absence of infection, sometimes behave as if they are infected and ultimately perish. Upon their death, they emit signals to surrounding cells, which can trigger those neighboring cells to also die. If researchers can uncover the origins of this lethal signaling, it may be possible to halt the chain reaction, thus aiding in the treatment of sepsis.

The enigma of this fatal signaling may now be clarified. It seems that the “messages” are generated as the cells attempt to survive, according to research from the UConn School of Medicine featured in Cell.

The chain reaction initiates with cells that are indeed infected. To curtail the spread of the infection, these cells commit cellular suicide by transporting a protein known as gasdermin-D to their outer membrane. Multiple gasdermin-D proteins cluster together, forming a pore in the cell’s surface akin to a punctured balloon. As a result, the cell’s inner contents leak out, leading to its demise.

However, not all is lost; some cells manage to respond quickly to eject the section of their membrane that contains the gasdermin-D pore. They then seal their membrane and survive. The expelled membrane transforms into a tiny bubble called a vesicle, which conveniently carries the dangerous gasdermin-D pore. This vesicle can then drift and, upon coming into contact with a nearby cell, can induce that cell’s membrane to rupture, leading to its death.

“When a dying cell releases these vesicles, they can pass on these pores to the surface of a neighboring cell, ultimately resulting in that cell’s demise,” explains Vijay Rathinam, an immunologist at UConn School of Medicine. Essentially, the harmful signals emitted are unintended consequences of cells attempting to save themselves. A cluster of dying cells can release a significant amount of gasdermin-D vesicles, leading to the death of numerous adjacent cells. This propagation of deadly signals exacerbates the escalating inflammation associated with sepsis.

Rathinam and his research team are currently investigating methods to reduce the effects of the harmful gasdermin-D vesicles. If they succeed, it could yield potential treatments for inflammatory disorders, such as sepsis.

This research, spearheaded by Skylar Wright, an MD/PhD student in Rathinam’s lab, was conducted in collaboration with the laboratories of Drs. Jianbin Ruan, Beiyan Zhou, Sivapriya Kailasan Vanaja from UConn Health, and Dr. Katia Cosentino from the University of Osnabrück, Germany. Funding for this project was provided by grants from the National Institutes of Health to Dr. Rathinam.