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Clinical Microbiology Reviews, October 2001, p. 689-703, Vol. 14, No. 4
0893-8512/01/$04.00+0   DOI: 10.1128/CMR.14.4.689-703.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Immune Responses in Hookworm Infections

Alex Loukas1,2,* and Paul Prociv3

Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, QLD 4006,1 and Australian Center for International Tropical Health and Nutrition,2 and Department of Microbiology and Parasitology,3 The University of Queensland, Brisbane QLD 4072, Australia

Hookworms infect perhaps one-fifth of the entire human population, yet little is known about their interaction with our immune system. The two major species are Necator americanus, which is adapted to tropical conditions, and Ancylostoma duodenale, which predominates in more temperate zones. While having many common features, they also differ in several key aspects of their biology. Host immune responses are triggered by larval invasion of the skin, larval migration through the circulation and lungs, and worm establishment in the intestine, where adult worms feed on blood and mucosa while injecting various molecules that facilitate feeding and modulate host protective responses. Despite repeated exposure, protective immunity does not seem to develop in humans, so that infections occur in all age groups (depending on exposure patterns) and tend to be prolonged. Responses to both larval and adult worms have a characteristic T-helper type 2 profile, with activated mast cells in the gut mucosa, elevated levels of circulating immunoglobulin E, and eosinoophilia in the peripheral blood and local tissues, features also characteristic of type I hypersensitivity reactions. The longevity of adult hookworms is determined probably more by parasite genetics than by host immunity. However, many of the proteins released by the parasites seem to have immunomodulatory activity, presumably for self-protection. Advances in molecular biotechnology enable the identification and characterization of increasing numbers of these parasite molecules and should enhance our detailed understanding of the protective and pathogenetic mechanisms in hookworm infections.

* Corresponding author. Present address: Department of Microbiology and Tropical Medicine, George Washington University, Ross Hall, 2300 Eye St., N.W., Washington, DC 20037. Phone: (202) 994-2671. Fax: (202) 994-2913. E-mail: mtmacl{at}gwumc.edu.

Clinical Microbiology Reviews, October 2001, p. 689-703, Vol. 14, No. 4
0893-8512/01/$04.00+0   DOI: 10.1128/CMR.14.4.689-703.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.