The study, conducted by researchers at the University of Las Palmas de Gran Canaria and the University of Salamanca, analyzed serum samples from 125 allergic patients living on Gran Canaria, an island considered hyperendemic for heartworm disease. Using enzyme-linked immunosorbent assays, the team measured two types of antibodies: immunoglobulin G (IgG) against both D. immitis somatic antigens and Wolbachia, an obligate bacterial endosymbiont of filarial nematodes, and immunoglobulin E (IgE) against D. immitis antigens. The results, published in Frontiers in Allergy, revealed that nearly one in four patients—23.2 percent—carried specific IgE antibodies against the parasite, a figure substantially higher than the 8.27 percent previously reported in the general population of the same region.

Humans are accidental, dead-end hosts for D. immitis. When mosquitoes carrying infective larvae bite a person, the parasites typically fail to reach sexual maturity and instead die in the pulmonary vasculature, producing the benign lung nodules classically associated with human dirofilariosis. But the researchers hypothesized that repeated exposure to larval antigens in hyperendemic areas might do something subtler: stimulate the immune system in ways that overlap with allergic inflammation, particularly in individuals whose immune responses are already biased toward a type 2 profile.

Type 2 immunity is the branch of the immune system that evolved to combat large multicellular parasites. It is characterized by eosinophilia, IgE production, mast cell activation, and cytokines such as interleukin-4, interleukin-5, and interleukin-13. These are precisely the same immunological features that drive allergic diseases like asthma, allergic rhinitis, and atopic dermatitis. The overlap raises a fundamental question: does helminth exposure protect against allergy by training regulatory circuits, or does it fuel allergic sensitization by providing additional antigenic stimulation? The answer, according to the study’s authors, likely depends on the parasite species, the intensity and chronicity of exposure, and the host’s immune background.

The most striking statistical finding in the new work was the association between peripheral eosinophilia and anti-D. immitis IgE seropositivity. Among patients whose eosinophil counts fell within the normal range, 14.9 percent tested positive for parasite-specific IgE. Among those with eosinophilia of 6 percent or higher, the figure jumped to 42.1 percent. Binary logistic regression confirmed that eosinophil status was the strongest predictor of IgE positivity, with individuals showing normal counts having substantially lower odds of seropositivity compared to those with elevated eosinophils (odds ratio 0.28, 95 percent confidence interval 0.10–0.72, p = 0.009). Fisher’s exact test further confirmed the association at p < 0.01.

Eosinophilia is a hallmark of both allergic inflammation and helminth-driven type 2 immune responses, making the association biologically plausible. However, the cross-sectional design of the study prevents any conclusion about causality. It remains possible that patients with an existing atopic constitution are simply more prone to mount IgE responses against parasite antigens. Alternatively, repeated exposure to D. immitis antigens delivered through mosquito bites might contribute to sustaining eosinophilic inflammation in sensitized individuals. Disentangling these possibilities will require longitudinal studies with matched control groups.

A second key finding involved IgG antibodies. Six point four percent of patients tested positive simultaneously for IgG against D. immitis somatic antigens and against the recombinant Wolbachia surface protein. Because humans are non-permissive hosts and the parasite rarely completes its life cycle, this dual positivity likely reflects contact with infective larvae and subsequent immune recognition of both nematode and endosymbiotic bacterial components. Wolbachia has long been implicated in the inflammatory pathology of filarial infections, driving neutrophil activation, release of inflammatory mediators, and IgG responses in human pulmonary dirofilariosis. In the context of allergic disease, such exposure may contribute to a broader inflammatory environment, although the specific contribution of Wolbachia to type 2 immune polarization remains to be clarified.

Gran Canaria offers a uniquely informative setting for this kind of investigation. The island sustains high rates of D. immitis transmission in dogs and cats, and its human population carries one of the highest allergic disease burdens in Spain, with asthma affecting 18.4 percent, rhinitis 40.3 percent, and atopic dermatitis 35.8 percent of residents. While factors such as African dust intrusions, pollen exposure, and climatic conditions have been proposed to explain this burden, the new findings suggest that vector-borne parasitic exposure may represent an additional, previously underappreciated contributor.

The authors acknowledge several important limitations. The IgE assay used a crude adult somatic antigen extract rather than purified or recombinant D. immitis-specific allergens, which are not currently available, making it impossible to identify the specific allergenic molecules driving the response. Cross-reactivity with other helminths or invertebrate pan-allergens, such as tropomyosins shared by mites and nematodes, cannot be excluded, particularly since all IgG/IgE-positive patients also showed sensitization to common environmental allergens. The study also lacked a contemporaneous non-allergic control group, relied on previously published data for population-level comparisons, and did not collect detailed epidemiological information about mosquito exposure, proximity to reservoir hosts, or repellent use. Furthermore, seropositivity indicates immunological exposure rather than active infection, and the small number of dual-positive patients limited statistical power.

Despite these caveats, the findings carry significant implications from a One Health perspective, linking animal reservoirs, mosquito vectors, and human immune responses within a single ecological framework. As climate change expands the geographic range of competent mosquito species and drives the spread of D. immitis across Europe, human dirofilariosis may need to be reconceptualized—not merely as a rare cause of pulmonary nodules, but as a potential contributor to occult allergic sensitization in endemic settings. The researchers call for controlled longitudinal studies, molecular allergen characterization, and careful assessment of cross-reactive mechanisms to determine whether this widespread veterinary pathogen is quietly shaping the allergic landscape of human populations living alongside it.

Subject of Research: Serological evidence linking Dirofilaria immitis exposure to allergic sensitization in a hyperendemic region

Article Title: Could Dirofilaria immitis contribute to occult allergic sensitization? Serological evidence from allergic patients in a hyperendemic area

Article References: Montoya-Alonso, J. A., Balmori-de la Puente, A., Rodríguez-Escolar, I., Collado-Cuadrado, M., Gil-Abad, A., Carretón, E., & Morchón, R. (2026). Could Dirofilaria immitis contribute to occult allergic sensitization? Serological evidence from allergic patients in a hyperendemic area. Frontiers in Allergy, 7, Article 1943450. https://doi.org/10.3389/falgy.2026.1943450

Image Credits: AI Generated

DOI: 10.3389/falgy.2026.1943450

Keywords: Dirofilaria immitis, heartworm, allergic sensitization, IgE, eosinophilia, Wolbachia, helminths, One Health, Gran Canaria, mosquito-borne disease, zoonosis, Frontiers in Allergy