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Galectin-1 may be a biomarker for patients at risk of life-threatening sepsis

Galectin-1, a sugar-binding protein, can trigger terrible inflammation and worsen sepsis, according to a team of researchers led by UConn Health in the January 4 issue of the journal Nature Immunology.


Editor: Akhmetova Aigerim
Author: Bolysbek Dana



Sepsis is most often caused by bacterial infections. The immune system gets out of control and triggers a cytokine storm - a condition in which inflammatory proteins fill the blood. Organs can fail, and death often follows.
Cytokine storms are also seen in patients with severe COVID-19 and are believed to be the cause of death in COVID-19.


The main trigger of cytokine storms during sepsis is an overreaction of the body when an infection is detected inside the cells. When a cell detects bacteria or parts of bacteria inside itself, it immediately activates enzymes, which in turn activate a protein that makes holes in the cell membrane from the inside, which eventually causes the cell to rupture and release cytokines into the bloodstream. Cytokines are alarms that call on the immune system to fight off bacteria. Cytokines also increase the likelihood of other cells exploding and triggering an alarm. Usually, after a while, the system calms down, but with sepsis, it gets out of control, causing more and more cells to die, releasing even more cytokines into the bloodstream.


When cells burst, they release not only cytokines, but also other dangerous molecules called alarmins, which alert the body to infection or injury and can amplify the ongoing cytokine storm.


UConn Health immunologist Vijay Rathinam wanted to know what kind of alarms are released when a cell detects a special kind of bacterial molecule called a lipopolysaccharide inside itself. Dr. Ashley Russo, in collaboration with immunologists Tony Vella and Antoine Menoret of UConn Health, catalogued the proteins released by these cells when they detected lipopolysaccharides.


So galectin-1, a protein that binds sugar and other sugar-coated proteins, was discovered. But galectin-1 was small enough to slip out of the holes in the cell membrane.


As soon as this was noticed, the study of the role of galectin-1 in the development of sepsis began. The researchers found that galectin-1 appears to inhibit the inhibition of inflammation, which leads to a build-up of the cytokine storm. Also, mice lacking galectin-1 had less inflammation, less organ damage, and survived longer than normal mice during sepsis caused by a bacterial infection.


It was found that patients with sepsis have higher levels of galectin-1 than other patients without sepsis.


The team is looking at whether galectin-1 could be a good therapeutic target to help mitigate cytokine storms during sepsis, as well as a useful marker that doctors could use to identify critically ill patients at risk.