Urocanic acid linked to a deadly parasite of the developing world

Researchers at the University of Pennsylvania have found a link between some of the world's most common parasites that cause infection and disease throughout the developing world and their attraction to a chemical secreted from human and animal skin.

These skin-penetrating parasites infect more than 600 million people worldwide and contribute to anemia, ill health and poor physical and cognitive development among children of developing nations.

Urocanic acid, a common histidine metabolite abundant in mammalian skin, attracts the parasitic nematode Strongyloides stercoralis.  But, according to researchers, the attraction can be suppressed by metal ions, suggesting a potential new strategy for preventing infection.

The findings were reported in the Proceedings of the National Academy of Sciences.  

Parasites travel by chemotaxis, the process frequently understood to direct cellular movement that relies upon chemical cues in the surrounding physiological environment.  Thus, in complex organisms, chemotaxis is critical to normal function; however, it is also the process by which many parasites find their hosts.  Although skin-penetrating nematodes like hookworms and threadworms are drawn to body heat, Penn researchers found that urocanic acid also serves as a "cue" for S. stercoralis.

More than identifying a critical component in the way parasites find hosts, the Penn study also revealed that metal ions could reduce the level of attraction between the parasites and the urocanic acid, potentially providing a new foundation to prevent nematode infection.  Researchers suggest that topical application of calcium, magnesium or manganese creams may reduce attraction levels.

The research supports some non-governmental organizations' advocacy of appropriate technology to develop inexpensive and practical treatments to prevent infections and to ward off parasitic diseases in poor, developing countries.

The study was performed by Daniel Safer from the Department of Physiology in Penn's School of Medicine and Gerhard Schad, Mario Brenes and Seth Dunipace from the Department of Pathobiology in Penn's School of Veterinary Medicine.

The study was funded by the National Institutes of Health


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