Allergic conditions have surged to unprecedented levels globally, affecting approximately 30% of the global population. Fungi are among the most significant sources of allergens, accounting for approximately 6% of respiratory issues in the general population. However, identifying the precise cause of respiratory allergies remains challenging. We investigated the potential of two rust species, Tranzschelia pruni-spinosae and Phragmidium rubi-idaei, which infect common fruit plants, to induce inflammatory and asthmatic responses in mouse models of both acute and chronic asthma. Mice were sensitized and administered intranasal challenges with extracts from T. pruni-spinosae and P. rubi-idaei. Levels of pro-inflammatory cytokines (IL-4, IL-5, IL-13, TNF-α, and TGF-β) were measured via ELISA. Additionally, specific IgE production was assessed via ELISA and lung histology was examined using hematoxylin-eosin staining. Both fungal extracts induced significant increases in all tested cytokines, elevated specific IgE levels, and histological changes characteristic of acute and chronic asthma progression in the lungs. The microfungi T. pruni-spinosae and P. rubi-idaei possess strong proinflammatory and asthma-inducing capabilities, suggesting their potential as previously unrecognized fungal allergens.

Allergic conditions have surged to unprecedented levels globally, affecting approximately 30% of the population. Fungi are among the major sources of allergens, accounting for about 6% of respiratory issues. Identifying the causes of respiratory allergies is not always possible. Our study assessed the capacity of two plant parasites, Podosphaera fusca and Peronospora ficariae, which infect Cucurbita pepo and Ficaria verna, to provoke inflammatory and asthmatic reactions in mouse models of acute and chronic asthma. We performed experiments by sensitizing mice through intranasal challenges with extracts from P. fusca and P. ficariae. Subsequently, we used ELISA tests to measure pro-inflammatory cytokines, including IL-4, IL-5, IL-13, TNF-α, and TGF-β. We evaluated specific IgE production through ELISA and examined histological changes in mouse lungs using hematoxylin-eosin staining. Our research revealed that P. fusca and P. ficariae induced significant production of all tested cytokines, increased specific IgE levels, and caused histological changes characteristic of acute and chronic asthma progression. Although weaker than the reference allergen ovalbumin, P. fusca and P. ficariae possess proinflammatory and asthma-inducing capabilities, indicating the potential to expand the current list of fungal allergens.

Fungal exposure and sensitization are linked to asthma severity, but their clinical significance varies by host, exposure context, and disease phenotype. This review integrates epidemiological, immunological, and clinical evidence on fungal-associated asthma, distinguishing environmental exposure, allergic sensitization, and persistent airway colonization. We examine how fungal allergens, proteases, and cell-wall components engage pattern-recognition receptors, disrupt epithelial barriers, and activate overlapping type 2 and type 17 inflammatory pathways. Studies of the airway and intestinal mycobiome offer additional perspectives on host–fungal interactions, although most human findings remain associative and do not establish causality or clinical utility. Severe asthma with fungal sensitization (SAFS) and allergic bronchopulmonary aspergillosis (ABPA) are distinct clinical contexts that require different diagnostic and therapeutic approaches. Antifungal treatment has an established role in ABPA, whereas evidence in SAFS is inconsistent; biologic selection should be guided by clinical phenotype and established eligibility criteria rather than fungal sensitization alone. We also synthesize our published biochemical, epithelial-cell, and murine studies of seven plant-associated fungal and oomycete taxa from eastern Poland. These findings support further investigation of their allergenic and pro-inflammatory potential but do not establish clinical allergenicity or predict treatment response in humans. Priorities include standardized exposure assessment, validated diagnostic reagents, and longitudinal studies linking fungal measurements to clinical outcomes. Expanded allergen panels and mycobiome-based approaches require prospective validation before routine clinical implementation.