In 2004, parasitologist David Pritchard applied a wet piece of gauze to his left forearm. This dressing contained an unknown number of hookworm larvae — 10, 25, 50, or 100. Pritchard and several other researchers, including his colleagues at the University of Nottingham (collectively, these scientists have devoted decades to studying this parasite around the world), infected themselves with this helminth. The immediate goals of this experiment were twofold: to determine how many helminths a 21st-century Briton could handle, and to prove that the aforementioned Briton was able to live with a certain number of helminths without symptoms of adverse effects-or at least that he would not die.
This project has caused many serious concerns. The Ethics Board was appalled. Even Pritchard’s wife was worried that he might be spreading parasites. However, Pritchard and his colleagues conceded that Necator americanus did not deserve its established reputation as a helminth that causes anemia, slows growth, and exacerbates poverty. They believed that hookworm could have therapeutic value as a method of treating allergic diseases. In a broader context, these scientists were looking for an answer to the question at the heart of modern allergy science: what exactly is an allergic reaction?
During the hay fever season, the antibody class immunoglobulin E (or IgE) causes such disasters as a runny nose, inflamed eyes, and incessant sneezing. In addition, it is these antibodies that contribute to the appearance of urticaria, spontaneous vomiting and deadly narrowing of the pharynx due to food allergies. It is this class of antibodies that is responsible for the fact that every year after a bee or wasp bite, several people have anaphylactic shock, their face swells, their blood pressure drops, and they die. If we assume that the manifestation of murderous rage against cat hair, birch pollen, or bee stings is not the “goal” of immunoglobulin E formed in the course of evolution, then one question remains: what is the purpose of IgE?
Class E antibodies are present in all mammals, including marsupials that separated from our genus 110 million years ago. Birds that went their own way 200 million years earlier have antibodies with similar functions-IgY. Therefore, IgE is an ancient antibody. They existed long before the appearance of the insect-eating shrew-like creature 100 million years ago. This creature was destined to become the ancestor of all placental mammals.
The persistence of these antibodies in mammals of all genera, as well as the presence of their functional counterpart in birds, implies that IgE plays an important role. However, since scientists identified these antibodies in the 60s, the meaning of their existence has remained unclear.
Immunoparasitologists, who approached this question from a completely different angle, for the first time formulated the reason for the existence of IgE. They suggested that Class E antibodies, which increase in number when infected with helminths, are actually one of the components of our parasite control system. However, although the high IgE content indicated a high prevalence of allergic diseases in places such as London and New York, there was no correlation between increased IgE content and allergic diseases in the populations whose members became carriers of helminths. In the blood of parasite carriers living in the tropics, there could be hundreds of times more IgE than in residents of London or New York suffering from hay fever. However, such people usually did not sneeze from dust, they did not develop hives due to hazelnuts, and they did not have allergies of any other type. Interestingly, in an environment with a high prevalence of helminths, the increased content of IgE was not associated with allergic diseases.
This observation led scientists to make the following assumptions: the protective mechanisms of these parasites can only work properly in the case of those helminths for which they were formed during evolution; perhaps the treatment of allergic diseases is reduced to artificially stimulating the level of IgE; maybe a living parasite is able to perform this task.
As you might expect, the latter idea caused a fierce debate. Pritchard’s experiment was the result of a certain weariness from the endless bickering about it. He believed that the best way to prove the ability of parasites to protect against all allergic diseases was to infect a person with an allergy with helminth, and (as he hoped) watch the allergy disappear. Of course, Pritchard hadn’t reached that stage yet. First, he had to prove the safety of this approach. Nevertheless, he was moving in this direction-towards the search for an unconventional method of treating allergic diseases.