David Pritchard knew this backstory when he first came to Karkar in the late 80s-a small island with an active volcano located about sixteen kilometers from Papua New Guinea. Pritchard wrote his doctoral dissertation on the topic of the intriguing relationship between helminths and an allergic reaction. However, he came to this lush island to explore a more fundamental aspect of the “parasite — host” relationship: how can one organism settle inside another and maintain a kind of peaceful coexistence with it, despite the fact that the rapidly reacting immune system is determined to kill it?
“In fact, no one really understood why the human body does not reject the helminth,” says Pritchard. — We went to Papua New Guinea to study people who were infected naturally.”
When Pritchard arrived on the island, many Papuans still led a predominantly rural lifestyle in the villages. In addition, almost all of them were infected with Necator americanus (the prevalence of this helminth was about 95%), as well as other parasites. In cases where the nature of the infection was not too severe, the Papuans lived in relative harmony with their snek bilong bel — “snakes in the stomach”. Pritchard and his team collected fecal samples, distributed drugs to expel worms, analyzed the parasitic load and measured antibody levels. Years passed. Since Pritchard spent a lot of time in the jungle, he had a lot of opportunities for reflection. Soon he began to doubt the truth of the prevailing immunological paradigm as a whole.
First, Pritchard was no longer so sure that the immune response that takes place in the case of helminth infection is really aimed at destroying parasites. It seemed that the immune response rather protects the host from itself. This dynamic is well illustrated by the condition known as” elephantiasis ” (elephant disease) — a painful hypertrophied swelling of a particular part of the body caused by a thread nematode. These helminths, which are carried by mosquitoes, live in the human lymphatic system. Most of the people who provide them with shelter do not show any symptoms. However, the immune system of some people undertakes a furious attack on helminths, and these unfortunate people develop a painful, disfiguring disease. Obviously, the “fire from all guns” approach can lead to the opposite results. The immune system sometimes becomes your worst enemy. Sometimes the best answer is tolerance.
Pritchard wasn’t the only one who raised such questions. Other researchers who studied groups of the population infected with helminths naturally began to think about who the increased level of IgE really benefits — the host or the parasite. Most of the IgE has no obvious connection with helminth proteins. This is more like a smoke screen, the deliberate erosion of the host’s defense by the worm — the immune equivalent of nonsense. Others believed that perhaps these so — called “polyclonal iges” represent a deliberate “self-clouding” of the host-a way to avoid a severe allergic reaction, sometimes killing people with an extremely high predisposition to allergies.
Pritchard found that people who produce more IgE than everyone else usually have weaker helminths. The parasites of such people were smaller and laid fewer eggs. Based on this observation, Pritchard came to the following conclusion: although the ability to produce a large amount of IgE in a helminth-infested environment has obvious advantages, people with such an innate ability who grew up in London are most likely to develop allergic diseases. “Allergy can be considered as an evolutionary ‘legacy of parasitism’, ” Pritchard wrote in 1997. And people with the worst heritage of this kind live best in an environment teeming with helminths.
The most important thing is that we are not doomed to allergic diseases. On the island of Karkar, allergies are relatively rare. As long as the helminth control tools remain in the proper context (in the context of parasite control), they do not create so many problems. And if we need contact with parasites in order to maintain the optimal functioning of the immune system, then these organisms, strictly speaking, are not parasites. They are mutuals.
Even in this case, Pritchard was not alone in his thoughts. Other scientists have also come to the conclusion that helminths can benefit their hosts in the most unexpected ways. Researchers from Thailand drew attention to the fact that carriers of giant roundworms are less at risk of cerebral malaria. Helminths do not provide direct protection against plasmodium, as the vaccine does. Rather, they restrain the host’s immune response, preventing the immune firestorm that leads to a predisposition to malignant malaria. (Other researchers have come to the same conclusion, but it is still controversial.)
In Australia, repeated cases of infection of people with the canine crooked head Ancylostoma caninum in the 90s highlighted another important point: only those helminths that have evolved together with humans provide benefits. Helminths that are new to humans can cause serious diseases. In this case, the hookworm that adapted to the dog successfully colonized a person, which indicates the formation of a new species. However, this parasite has settled in a person not very delicately. Unlike human hookworm, canine helminths cause severe inflammation, ulcers and enteritis.
In Japan, outbreaks of anisakidosis caused by helminths from undercooked or raw fish also illustrate this idea. Helminth from the anisakid family (herring worm), which lives in seals and dolphins, can cause serious symptoms and even life-threatening diseases in humans. It is obvious that these parasites do not know how to behave in the human body. All this highlights the fact that N. americanus and other parasites that have adapted to humans are really unique. What can they teach us about how the human immune system works? Can they reveal to us information about the treatment of the epidemic of allergic diseases in developed countries through a secret protein or enzyme?
All these are pressing issues. Meanwhile, in the period from the middle to the end of the 90s, Pritchard had not yet considered the possibility of deliberately infecting a person with N. americanus helminth. However, a number of studies conducted in Africa changed his opinion.