Stories about: infection

Self-sacrificing cells hold clues to improving treatment of MRSA, sepsis

Image of neutrophils
During infection, white blood cells called neutrophils eject their own DNA strands outward to block bacteria from spreading. IMAGE: ADOBE STOCK

Over the last several years, scientists have made great headway in our understanding of how self-sabotaging immune cells play a role in our ability to fight infection. So far, we know that when white blood cells called neutrophils are triggered by bacterial infection, they self-combust and eject their own DNA strands outward like spider webs. Sacrificing themselves, the exploded neutrophils and their outreaching DNA tentacles form sunburst-shaped neutrophil extracellular traps (NETs).

“NET formation is an innate immune response that our body has when it recognizes the presence of pathogens,” says Ben Croker, PhD, a researcher in the Division of Hematology/Oncology at Boston Children’s Hospital. “Once formed, NETs restrict pathogen movement and proliferation and alert the rest of the immune system to the invader’s presence.”

Now, Croker and a team of researchers at Boston Children’s have identified a critical element of NET formation and how it enables the body to fight off infections like methicillin-resistant Staphylococcus aureus (MRSA). Their findings, recently published in Science Signaling, could someday have clinical implications for tough-to-treat infections and even sepsis.

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Blood filtration device could provide personalized care for sepsis

Artistic image of cytokines
Could cell-signaling proteins called cytokines be modulated to tame inflammation? IMAGE: ADOBE STOCK

Cytokines are small proteins produced by the body’s cells that have a big impact on our immune system. Researchers at Boston Children’s Hospital believe that modulating their presence in our bodies could be the key to improving outcomes in life-threatening cases of trauma, hemorrhage and many other conditions including sepsis, which alone impacts nearly one million Americans each year.

The reason? Cells essentially use cytokines to talk to one another. In response to their surroundings, cells release different types of cytokines that encourage inflammatory or anti-inflammatory effects on the body. Infection or trauma causes cells to pump out more cytokines that produce inflammation. Altogether, an escalating chorus of cytokines can sometimes tip a person’s body into overwhelming inflammation that can turn fatal, which is what happens during sepsis.

But what if scientists could remove the problematic cytokines to bring the choir into perfect tune, allowing the immune system to respond with just the right amount of inflammation for healing?

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News Note: Modeling sepsis better to find a cure faster

In this SEM image, E. coli (green) bacteria, a common instigator of sepsis, is captured by bioengineered magnetic beads.
New assessment criteria for monitoring sepsis in pig models could help clinical researchers more accurately evaluate potential sepsis treatments in preclinical experiments. In this SEM image, E. coli (green) bacteria, a common instigator of sepsis, is captured by bioengineered magnetic beads. Credit: Wyss Institute at Harvard University

Sepsis, or blood poisoning, occurs when the body’s response to infection damages its own tissues, leading to organ failure. It is the most common cause of death in people who have been hospitalized, yet no new therapies have been developed in the last 30 years. Many treatments that have prevented death in animal experiments have failed in clinical trials, indicating that a more clinically-relevant sepsis model is needed for therapeutic development.

To bridge this gap, a team of scientists from the Wyss Institute at Harvard University and Boston Children’s Hospital think a better experimental model of sepsis in pigs could help weed out the therapies most likely to succeed in humans. Their method, a scoring criteria to evaluate sepsis in pigs that closely mirrors standard human clinical assessment, is reported in Advances in Critical Care Medicine.

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