Biology subjects

Liaghat, A.

Publications and source records attributed to Liaghat, A..

3 recordsLinked to original sources

bioRxiv2026

Development and translational validation of a novel mouse model for allergic rhinitis

Background: Approximately 30% of the North American population are affected by seasonal or perennial rhinitis. Allergens from cats are common triggers of allergic rhinitis. Importantly, cat allergic rhinitis (cat-AR) is a major risk factor for more severe allergic diseases, including asthma. Current therapies rarely achieve full symptom control and development of novel therapeutics is constrained by the lack of physiologically relevant preclinical models. Objective: Establishment of a clinically-informed mouse model of cat allergen exposure in humans. Methods: Controlled human exposure was performed using airborne natural cat dander (CD) in a validated environmental exposure facility. Nasal immune cells and IgE concentrations in serum and nasal samples were assessed. In mice, we established a 14-day intermittent intranasal sensitization and challenge protocol using the same CD allergens. Clinical signs in mice were objectively quantified using AI-based video detection. Cellular changes in the nose were assessed with level-specific, spatial resolution. Lastly, systemic sensitization was confirmed through serum IgE and intradermal ear challenge. Measurements and Main Results: Following CD exposure, cat-allergic participants displayed increased nasal symptoms and eosinophil influx. CD-sensitized mice recapitulated key clinical features, including increased nasal rubbing, elevated nasal immune cell infiltration, and systemic sensitization. Importantly, spatial investigation of the cellular changes revealed major changes in the turbinate and olfactory regions of the nose. Conclusions: This novel mouse model provides a translationally valuable platform for investigating local and systemic mechanisms of cat-AR. It will serve for mechanistic and therapeutic evaluations with the goal of improving clinical translation and therapeutic precision.

immunology↗

bioRxiv2026

Tipping points are typical in ecosystems with higher-order interactions

Whether species-rich communities erode gradually or collapse abruptly under environmental change is a central question in ecology [1]. Classical pairwise theory predicts that coexistence is always lost gradually, through smooth declines to extinction [2], yet real ecological interactions are often strongly state-dependent - shaped by nonlinearities that fixed pairwise coefficients cannot capture [3]. Here we show that higher-order (nonlinear) interactions make abrupt, irreversible loss of coexistence a typical route to community collapse: across diverse random communities, the equilibrium supporting coexistence disappears suddenly at a fold bifurcation. Using polynomial homotopy continuation [4] to track equilibria as environmental conditions change, we find that folds progressively dominate the boundary of the coexistence domain as nonlinearity strengthens, replacing the gradual extinctions of pairwise theory. Furthermore, the sign structure of higher-order interactions controls both the onset of tipping-points and whether biodiversity buffers or amplifies collapse. Because higher-order and nonlinear interactions are intimately linked, tipping points also arise generically in pairwise models with strong nonlinearity. Applying our continuation framework to a canonical model of plant-pollinator collapse [5], we formally resolve its bifurcation structure as fold-mediated, and we show that fold bifurcations are typical across published multispecies models spanning mutualistic, competitive, and consumer-resource interactions. These results challenge the expectation that monitoring abundances suffices to anticipate collapse, and unify structural-stability theory, which delineates the safe operating space for coexistence, with critical transition theory, which characterizes the nature of its boundaries.

ecology↗

bioRxiv2025

Host Competitive Asymmetries Accelerate Viral Evolution in a Microbe-Virus Coevolutionary System

Microbial host populations evolve traits conferring specific resistance to viral predators via various defense mechanisms, while viruses reciprocally evolve traits to evade these defenses. Such co-evolutionary dynamics often involve diversification promoted by negative frequency-dependent selection. However, microbial traits conferring competitive asymmetries can induce directional selection, opposing diversification. Despite extensive research on microbe-virus co-evolution, the combined effect of both host trait types and associated selection remains unclear. Using a CRISPR-mediated co-evolutionary system, we examine how the co-occurrence of both trait types impacts viral evolution and persistence, previously shown to be transient and non-stationary in computational models. A stochastic model incorporating host competitive asymmetries via variation of intrinsic growth rates reveals that competitively-advantaged host clades generate the majority of immune diversity. Greater asymmetries extend viral extinction times, accelerate viral adaptation locally in time, and augment long-term local adaptation. These findings align with previous experiments, and provide further insights into long-term co-evolutionary dynamics.

evolutionary biology↗