Experimental Hematology

Gene loss impaired movement of immune cells from mice

In laboratory tests, immune cells from genetically altered mice moved less effectively toward a chemical signal than cells from control mice.

Our read

Mechanisms
Studied:
Experiments in bone marrow neutrophils from mice, against wild-type controls
What changed:
Bone marrow neutrophils lacking Dnmt3a showed impaired migration compared to wild-type controls
The catch:
Vav-Cre mice carry a Commd10 mutation that may independently alter inflammatory responses
In the record:
One of 292 papers on DNMT3A on record: 40 with results in people, 19 in animals.

Editor of record: Boris Djordjevic · AgingResearch.News

Follow @agingbrief

Mice engineered to lack the Dnmt3a gene accumulated more influenza A virus in their lungs than age- and sex-matched controls in an animal experiment. Researchers infected the mice through the nose and assessed lung virus and immune cells 40 hours later.

The deficient mice had fewer neutrophils, immune cells that help fight infection, in infected lungs despite comparable numbers in the blood. In laboratory tests, neutrophils from deficient mice moved less effectively toward a chemical signal than control cells. Their maturation, levels of germ-killing enzymes and measured capacity to produce energy were unchanged. Gene activity linked to cell movement and immune signaling was reduced. At the tested infection dose, gene loss did not change mortality or weight loss.

Why it matters

Clonal hematopoiesis, an age-related expansion of blood cells carrying acquired mutations, is linked to severe infections. The work offers a possible mechanism for that vulnerability.

Caveats

The movement tests used isolated mouse cells. The experiments tested gene deletion rather than the age-related expansion of mutated blood-cell groups that occurs in people.

Comments

Be the first to comment.