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Basophil competence during hookworm (Necator americanus) infection
David I Pritchard1, Doreen S W Hooi, Alan Brown
1The Boots Science Institute, School of Pharmacy, University of Nottingham, University Park, Nottingham, United Kingdom.
The American Journal of Tropical Medicine and Hygiene
|November 7, 2007
Summary
Parasites may survive by blocking immune responses. However, this study found that basophils in hookworm-infected individuals remained functional, suggesting their immune cells are not blocked.
Area of Science:
- Immunology
- Parasitology
Background:
- Helminth infections often induce a T helper 2 (Th2) immune response.
- A hypothesis suggests parasite survival is due to Fc epsilonRI blockade by IgE, preventing immune cell activation.
- This blockade is thought to involve parasite-induced polyclonal IgE.
Purpose of the Study:
- To investigate basophil function in a helminth-parasitized population.
- To test the hypothesis that Fc epsilonRI-bearing cells are refractory to activation during parasitic infection.
Main Methods:
- Studied 43 individuals from a hookworm-endemic area.
- Assessed basophil histamine release in response to various agonists.
- Measured total IgE levels and eosinophilia.
Main Results:
- Individuals exhibited high total IgE and eosinophilia, with a significant hookworm burden.
- Basophils from all participants released histamine when stimulated with anti-IgE and a hookworm allergen (calreticulin).
- Fc epsilonRI blockade on basophils was not observed.
Conclusions:
- The findings indicate that Fc epsilonRI blockade on basophils does not occur in this hookworm-infected population.
- This suggests that the effector functions of basophils, an arm of the Th2 response, remain active despite parasitic infection.
