WASHINGTON (June 1, 2011) By using mice lacking a crucial gene that controls the process of chromatin remodeling of cytokines including those responsible for inflammation and comparing them to normal wild type mice with the gene, researchers at the George Washington University School of Medicine and Health Sciences have shown that the gene, Mta1, is essential for the parasite Schistosoma haematobium to establish a productive infection and survival in the host.
Schistosomes are flukes (helminth worms) that can infect people when they come into contact with water carrying the parasite. They proliferate and cause chronic inflammation and fibrosis in the liver, and many migrate to the bladder, causing inflammation, granulomas, and eventually, bladder cancer. S. haematobium is responsible for two-thirds of the world's 200 to 400 million cases of human schistosomiasis, resulting in an estimated 280,000 deaths per year.
Publishing in the July issue of the journal Hepatology, the researchers demonstrated the role of Mta1, the metastasis-associated protein-1 (MTA1) gene, in the survival of schistosomes. They infected two strains of mice with schistosome cercariae, a larval stage of the parasite, by immersing their tails in water containing cercariae, from which the cercariae penetrated the skin. The wild type mice had the intact Mta1 gene, and Mta1-/- mice lacked the gene but were normal in other respects.
At various times after infection, blood was taken from the portal circulatory system of the liver to look for worms, and parasite eggs were quantified from the liver tissue. "At the twelfth week of infection we found that the wild type mice, that is, the mice in which the gene was intact, had severe granulomatous lesions in the liver. The worm count was very high, and in the mice that did not have the gene, we did not have any worms. Neither did we have any eggs that we could collect from the portal perfusion," said lead author Suji
|Contact: Anne Banner|
George Washington University Medical Center