COLUMBUS, Ohio - A new study in mice suggests that a treatment using a specific type of immune cell can eradicate the ulcer-causing bacteria Helicobacter pylori.
The research found that mice with deficient immune systems completely recovered from infections with H. pylori after they were treated with healthy spleen cells. After that treatment, no trace of the bacteria was found in the stomachs of these mice.
"These mice initially had a quick and severe reaction to the ulcer-causing bacteria," said Kathryn Eaton, a study co-author and an associate professor of veterinary biosciences at Ohio State University. "But the reaction was completely reversed in a matter of months, and the bacteria also disappeared."
The research appears in a recent issue of the journal Infection and Immunity. Eaton co-authored the study with Megan Mefford, a research assistant at Ohio State.
Scientists know that H. pylori causes stomach ulcers inhumans. The body typically responds to the bacterial infection with a condition called gastritis, an inflammation of the stomach lining. Antibiotics help control the growth and spread of the bacteria, but medication doesn't always completely eliminate it. And while gastritis may help control H. pylori levels, it can also damage the stomach.
"Once infected, people appear to remain infected for life," she said. "Even with medical intervention, the bacteria may persist or recur. We want to figure out how to eliminate a highly resistant pathogen that the animal or human normally can't eliminate."
The researchers compared the levels of H. pylori in six groups of mice: two sets of healthy mice and four sets of immune-deficient mice. At the beginning of the study, half of the healthy mice were infected with H. pylori. Two of the immune-deficient groups were also infected with H. pylori, and half of these mice were injected with splenocytes - spleen cells taken from healthy mice. Spleen cells normally help the blood filter toxins and foreign invaders from the body.
The researchers wanted to assess the effect of the spleen cells in the infected, immune-deficient mice. Immune-deficient mice lack mature spleen cells. Also, H. pylori causes only gastritis, not ulcers, in mice. The mice were sacrificed at 12 different intervals during the 51-week study.
One day before the animals were sacrificed, the researchers injected 10 micrograms of H. pylori into one hind footpad of each mouse and sterile saline into the opposite footpad. The researchers looked for subsequent swelling that would indicate the body's response to the infection. They recorded the thickness of each footpad 24 hours later. After sacrifice, the researchers removed and dissected the stomachs of each mouse in order to determine bacterial colonization.
The immune-healthy mice that had been infected with H. pylori had significant gastritis by 16 weeks when compared to healthy, uninfected mice. And gastritis continued to develop during the course of the 51-week experiment.
However, the immune-deficient mice injected with healthy spleen cells experienced a reversal, and eventual disappearance, of gastritis. This suggests that the healthy, mature spleen cells helped clear the animals' stomachs of the bacteria.
"The persistence of H. pylori in the healthy mice was consistent with extensive evidence in humans and other animals that the body's immune response - gastritis - fails to eliminate the bacteria," Eaton said.
While the mice that received the splenocytes also developed gastritis, they began to recover by 31 weeks (about seven months) and, by 45 weeks (about 10 months), the stomachs of those mice looked normal.
"If we can determine what subsets of the immune system are important for getting rid of the bacteria in mice, then we could look at two types of people: those who are infected but who don't get sick, and infected individuals who do develop illness," Eaton said.
This research was supported in part by public health service grants from the National Institutes of Health.
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