Researchers with the Iowa City VA Health Care System and University of Iowa have produced striking new evidence of neutrophil plasticity, or the ability of these white blood cells to change their properties.

The scientists exposed neutrophils to Helicobacter pylori bacteria. The lab experiments are among the first to show how mature white blood cells can change while still alive, in response to bacteria.

"Changes in neutrophil phenotype and function have been observed before, but only in vivo – such as in the circulation of sepsis patients, or in the joints of persons with arthritis," said study senior investigator Dr. Lee–Ann H. Allen. "However, previous attempts to reproduce these phenotypes using neutrophils isolated from human blood have not been successful. Thus, our study is the first to show that H. pylori infection, on its own, can alter the phenotype of human neutrophils."

"Our study is the first to show that H. pylori infection, on its own, can alter the phenotype of human neutrophils." Allen and her colleagues say the new findings may lead to a better understanding of how bacterial diseases arise in the body and how white blood cells respond. The scientists believe this may pave the way for new treatments, especially in the area of gastric health.

The results appeared March 1, 2017, in the Journal of Immunology.

The neutrophil cells exposed to H. pylori underwent structural changes. The nucleus of a normal neutrophil cell usually has three or four interconnected lobes. But when infected with H. pylori, the neutrophil nuclei showed six or more lobes per cell.

Such "hypersegmentation" is rare in neutrophils. According to the researchers, it shows the bacteria are actively changing the neutrophils through a direct interaction. Hypersegmentation was not seen when the researchers exposed eosinophils, a different type of white blood cell, to H. pylori. Also, the change only happened when neutrophils were directly infected with H. pylori, rather than when the bacteria were merely present. Neutrophils exposed to E. coli did not develop hypersegmentation, suggesting the change could be specific to H. pylori.

The bacteria also change the neutrophils in other ways, the study found. Normal neutrophils die as part of a natural process. But infected cells lived longer. The infected neutrophils also released molecules that are toxic to surrounding cells. When neutrophils are functioning normally, they produce chemicals called reactive oxygen species (ROS) around bacteria to kill the infection. H. pylori manipulates neutrophils so that they release ROS into the space outside the cells instead. This damages the stomach cells and helps the infection survive and spread.

The new study is the first lab demonstration of bacteria manipulating mature neutrophils. The authors say the work highlights the intriguing properties of these immune cells. They write, "Our findings are noteworthy as there is convincing evidence that neutrophils have multiple and potentially paradoxical roles in the development and progression of gastric disease."