Davies Lab
Davies Lab

The Problem

Helminths, or parasitic worms, including nematodes, flukes and tapeworms, collectively infect approximately 2 billion people worldwide, or about a third of the world’s population. The majority of infected people reside in developing countries in tropical and temperate climates, where helminths remain a significant public health concern and hamper socioeconomic development. Blood flukes of the genus Schistosoma are particularly prevalent in much of the developing world, with at least 250 million people infected with parasites that cause severe liver, intestine, and urogenital system pathology. In visitors from non-endemic areas, such as U.S. service personnel, schistosomes can cause an acute febrile illness that can be life-threatening. There is no vaccine or drug treatment that can prevent schistosomiasis, and only one partially effective drug is available to treat established infections.

Inside the Lab

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our Approach

The long-term objective of our studies is to develop new immunotherapies and chemotherapies aimed at inhibiting schistosome development in the human host, thus simultaneously preventing the pathology associated with schistosome infection and blocking parasite transmission. Our studies using a mouse model of Schistosoma mansoni infection have demonstrated that, paradoxically, schistosomes require signals from host immune cells to complete their development normally, suggesting that blocking interactions between schistosomes and host cells might provide a novel approach to interfere with parasite development. Currently we are focused on further understanding how schistosomes interact with host immune cells and how host responses modulate schistosome signal transduction and gene expression.

 

"Of all the forms of inequality, injustice in health is the most shocking and inhuman."

DR. MARTIN LUTHER KING
MARCH 25, 1966

Getting Results

Using immunodeficient mouse models, we were the first to show that all species of Schistosoma require host CD4+ T cells in order to develop normally. We have since shown that interleukin 4 (IL-4), a T cell-derived cytokine, can by itself support normal schistosome development in the absence of CD4+ T cells. These findings contribute to defining precisely how schistosomes take advantage of the environment inside their hosts to further their own replication and transmission, and point to new opportunities to disrupt the schistosome life cycle.

By analyzing schistosome-immune system interactions during the early stages of infection, we have identified schistosome proteins that induce pathogenic TH17 immune responses. These findings identify yet another mechanism by which schistosomes cause pathology, and one that may be especially relevant to understanding the development of acute schistosomiasis in service personnel.

By comparing schistosomes from normal mice with developmentally impaired schistosomes from immunodeficient mice, we have identified significant alterations in signaling pathways that control parasite metabolism. These findings suggest that schistosome metabolism is regulated in response host immune signals. We have also identified essential components of the parasite’s metabolic regulatory network that could be developed as targets for new drugs.

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