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Photo courtesy of Stuart Hay/
Australian National University
Scientists have identified a gene that could potentially aid the development of new treatments for sepsis.
The team knew that sepsis occurs when lipopolysaccharides (LPS) on the surface of some bacteria infiltrate cells, triggering an immune response that causes the cells to self-destruct.
However, it was unclear exactly how this happens. That is, until the team found the protein gasdermin D plays a critical role in the pathway to sepsis.
“This finding is a key that could potentially unlock our ability to shut down this killer disease before it gets to a life-threatening stage,” said Chris Goodnow, PhD, of The Australian National University in Canberra.
Dr Goodnow and his colleagues described their discovery in Nature.
The scientists found that gasdermin D usually exists in cells in an inactive form.
But when the LPS molecules enter cells, they trigger caspase-11 to lop off the protective chemical cap of gasdermin D. This, in turn, prompts the cells to self-destruct.
The team said this suggests gasdermin D is a critical target of
caspase-11 and a key mediator of the host response against Gram-negative
bacteria.
To identify the source of this discovery, the scientists screened thousands of genes. In a little over a year, they isolated the gene that produces gasdermin D.
Lead study author Nobuhiko Kayagaki, PhD, of Genentech in San Francisco, California, said this work could have implications beyond sepsis.
“The identification of gasdermin D can give us a better understanding not only of lethal sepsis, but also of multiple other inflammatory diseases,” he said. 
with a multi-pipettor
Photo courtesy of Stuart Hay/
Australian National University
Scientists have identified a gene that could potentially aid the development of new treatments for sepsis.
The team knew that sepsis occurs when lipopolysaccharides (LPS) on the surface of some bacteria infiltrate cells, triggering an immune response that causes the cells to self-destruct.
However, it was unclear exactly how this happens. That is, until the team found the protein gasdermin D plays a critical role in the pathway to sepsis.
“This finding is a key that could potentially unlock our ability to shut down this killer disease before it gets to a life-threatening stage,” said Chris Goodnow, PhD, of The Australian National University in Canberra.
Dr Goodnow and his colleagues described their discovery in Nature.
The scientists found that gasdermin D usually exists in cells in an inactive form.
But when the LPS molecules enter cells, they trigger caspase-11 to lop off the protective chemical cap of gasdermin D. This, in turn, prompts the cells to self-destruct.
The team said this suggests gasdermin D is a critical target of
caspase-11 and a key mediator of the host response against Gram-negative
bacteria.
To identify the source of this discovery, the scientists screened thousands of genes. In a little over a year, they isolated the gene that produces gasdermin D.
Lead study author Nobuhiko Kayagaki, PhD, of Genentech in San Francisco, California, said this work could have implications beyond sepsis.
“The identification of gasdermin D can give us a better understanding not only of lethal sepsis, but also of multiple other inflammatory diseases,” he said.
with a multi-pipettor
Photo courtesy of Stuart Hay/
Australian National University
Scientists have identified a gene that could potentially aid the development of new treatments for sepsis.
The team knew that sepsis occurs when lipopolysaccharides (LPS) on the surface of some bacteria infiltrate cells, triggering an immune response that causes the cells to self-destruct.
However, it was unclear exactly how this happens. That is, until the team found the protein gasdermin D plays a critical role in the pathway to sepsis.
“This finding is a key that could potentially unlock our ability to shut down this killer disease before it gets to a life-threatening stage,” said Chris Goodnow, PhD, of The Australian National University in Canberra.
Dr Goodnow and his colleagues described their discovery in Nature.
The scientists found that gasdermin D usually exists in cells in an inactive form.
But when the LPS molecules enter cells, they trigger caspase-11 to lop off the protective chemical cap of gasdermin D. This, in turn, prompts the cells to self-destruct.
The team said this suggests gasdermin D is a critical target of
caspase-11 and a key mediator of the host response against Gram-negative
bacteria.
To identify the source of this discovery, the scientists screened thousands of genes. In a little over a year, they isolated the gene that produces gasdermin D.
Lead study author Nobuhiko Kayagaki, PhD, of Genentech in San Francisco, California, said this work could have implications beyond sepsis.
“The identification of gasdermin D can give us a better understanding not only of lethal sepsis, but also of multiple other inflammatory diseases,” he said.