Global issues in allergy and immunology: Parasitic infections and allergy

Abstract

Allergic diseases are on the increase globally in parallel with a decrease in parasitic infection. The inverse association between parasitic infections and allergy at an ecological level suggests a causal association. Studies in human subjects have generated a large knowledge base on the complexity of the interrelationship between parasitic infection and allergy. There is evidence for causal links, but the data from animal models are the most compelling: despite the strong type 2 immune responses they induce, helminth infections can suppress allergy through regulatory pathways. Conversely, many helminths can cause allergic-type inflammation, including symptoms of "classical" allergic disease. From an evolutionary perspective, subjects with an effective immune response against helminths can be more susceptible to allergy. This narrative review aims to inform readers of the most relevant up-to-date evidence on the relationship between parasites and allergy. Experiments in animal models have demonstrated the potential benefits of helminth infection or administration of helminth-derived molecules on chronic inflammatory diseases, but thus far, clinical trials in human subjects have not demonstrated unequivocal clinical benefits. Nevertheless, there is sufficiently strong evidence to support continued investigation of the potential benefits of helminth-derived therapies for the prevention or treatment of allergic and other inflammatory diseases.

Regulation of immunity and allergy by helminth parasites

“…Indeed, there are many instances of sensitization and allergic reactions to parasites, particularly where zoonotic transmission occurs and the human is not the definitive host. 45,46 Examples are Toxocara canis, a canine nematode in which larval forms migrate through tissues of humans who have accidently ingested eggs, 47 and Anisakis simplex, a marine nematode which can be acquired by eating undercooked fish. 48 However, in both cases these are "dead-end" infections in which parasites are maladapted to the human and so fail either to complete their life cycle or down-modulate host immune reactivity.…”

Parasites and allergy: Observations from Brazil

“…However, a randomized controlled trial to study the possibility of increased susceptibility to STH parasites among allergic patients receiving anti‐IgE treatment was unable to identify evidence of increased susceptibility to STH infections among patients receiving anti‐IgE . The same concerns, however, are relevant for the use of new biological drugs (eg, anti‐IL‐5) targeting different components of type 2 inflammatory pathways …”

“…Similarly, improvements in sanitation and access to antiparasitic drugs have had dramatic effects on the prevalence of soil‐transmitted helminth parasites (STH), mainly Ascaris lumbricoides ( A. lumbricoides) , Trichuris trichiura (T. trichiura) and hookworm ( Ancylostoma duodenale and Necator americanus ), that were formerly highly prevalent in regions of Brazil with poor access to sanitation and clean water . The potential effects of a reduction in STH prevalence on asthma and atopy have been explored in some detail recently …”

“…25 The potential effects of a reduction in STH prevalence on asthma and atopy have been explored in some detail recently. 26 It has been suggested that parasites such as STH may induce immune regulatory mechanisms in the host and ameliorate aberrant immunological responses that are considered to underlie atopic 27,28 and autoimmune diseases. 29 The host inflammatory response to parasitic helminths such as STH and schistosome parasites and that documented for atopic conditions have many parallels including a systemic eosinophilia and elevated serum IgE, both of which are hallmarks of a type 2 immune response.…”

Isolated Schistosoma mansoni eggs prevent allergic airway inflammation

“…has also been reported to be protective against allergic sensitization in humans. 9,11 Schistosoma ssp. infections consist of an acute phase dominated by a strong Th2 response to the eggs and a chronic phase with a diminished Th2 response and increased activity of regulatory immune cells.…”