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Research Proving Single Enzyme Helping Drive Inflammation In Mice

Research Proving Single Enzyme Helping Drive Inflammation In Mice
Research Proving Single Enzyme Helping Drive Inflammation In Mice
R&D

Research study showing that the single enzyme helping drive inflammation in mice; providing the target for new sepsis drugs. As sepsis occurring when the body going overboard in its attempt to fight off an infection. Immune cells rush in, overreact and wreak havoc on tissues and organs; often resulting in organ failure and death. Inflammation is an essential aspect of innate immunity but also contributes to diverse human diseases.

But study recently finding that removing the enzyme PHLPP1 improving outcomes in a mouse model of sepsis. PHLPP1 controls many cell behaviors by removing phosphates (small chemical tags) from other proteins. And, it now turns out, PHLPP1 also influences inflammation. This introducing that the possibility that inhibiting PHLPP1 could form the basis for new sepsis treatments in humans.

Inflammation in mice

Most research on inflammation has typically focusing on the kinases, enzymes that add phosphate tags to other proteins, saying by the senior author in the research study professor in the Department of Pharmacology at UC San Diego School of Medicine. It is exciting to have a completely new target for sepsis the enzymes that remove them. PHLPP1 a few years ago and have since detailed its role in suppressing tumors.

Together, their teams uncovered many immune cell genes that are influenced by PHLPP1. But PHLPP1’s particular influence on inflammation could be linked to the fact that it removes phosphates from a transcription factor called STAT1, which is known for controlling inflammatory genes. Newton’s team took mice modified to lack the PHLPP1 gene to another UC San Diego School of Medicine colleague, Victor Nizet, MD, an expert on bacterial infections.

New target for sepsis

In separate experiments, Nizet’s team administered live E. coli bacteria and lipopolysaccharide (LPS), a component of the bacterium’s cell wall that drives immune systems wild; to both PHLPP1-deficient and normal mice. The difference surprised Newton: Mice without PHLPP1 fared much better. While all normal mice died of the infection-induced sepsis after five days, half of the PHLPP1-deficient mice survived.

Newton’s team had already been working with additional collaborators; to screen thousands of chemical compounds to identify those few that inhibit PHLPP1. Now that they know PHLPP1 inhibitors might form the basis for new anti-sepsis drugs, the researchers hope to test these compounds on immune cells in the lab and in the mouse model of sepsis. Currently, sepsis is addressed by preventing and treating the source infection; often with antibiotics, while maintaining organ health with oxygen and intravenous fluids.