How does allergy progress in rats? - briefly
Allergic responses in rats develop through an initial sensitization phase, during which antigen exposure induces IgE production, followed by a challenge phase that triggers mast‑cell degranulation and measurable airway inflammation. The progression is marked by a rapid increase in histamine, eosinophil infiltration, and bronchial hyperresponsiveness within hours to days after the second exposure.
How does allergy progress in rats? - in detail
Allergic disease in rats follows a predictable sequence that can be divided into three principal stages: sensitization, early‑phase response, and late‑phase response. During sensitization, repeated exposure to a specific allergen, typically administered intraperitoneally or via the airway, induces antigen‑specific IgE production by B‑cells under the influence of Th2‑derived cytokines such as interleukin‑4 (IL‑4) and interleukin‑13 (IL‑13). Antigen presentation by dendritic cells to naïve CD4⁺ T‑cells drives the Th2 polarization essential for IgE class switching. The resulting IgE circulates bound to high‑affinity FcεRI receptors on mast cells and basophils, establishing a primed effector pool.
The early‑phase reaction commences within minutes of allergen re‑exposure. Cross‑linking of IgE‑FcεRI complexes triggers rapid degranulation of mast cells, releasing histamine, tryptase, and platelet‑activating factor. Vascular permeability increases, leading to edema, while smooth‑muscle contraction produces bronchoconstriction in pulmonary models. Measurable outcomes include elevated plasma histamine levels, increased airway resistance, and reduced oxygen saturation, typically recorded within 5–30 minutes post‑challenge.
The late‑phase response emerges 4–24 hours after the initial trigger. Recruited eosinophils, neutrophils, and macrophages infiltrate the affected tissue, guided by chemokines such as eotaxin (CCL11) and cytokines including IL‑5 and tumor‑necrosis factor‑α (TNF‑α). This cellular influx sustains inflammation, promotes tissue remodeling, and may lead to fibrosis in chronic settings. Quantitative assessments involve bronchoalveolar lavage fluid (BALF) cell counts, histological scoring of eosinophilic infiltration, and measurement of cytokine concentrations by ELISA or multiplex assays.
Experimental protocols often employ ovalbumin or house‑dust‑mite extracts as model allergens. Sensitization schedules range from a single high‑dose injection to multiple low‑dose exposures over 7–14 days, depending on the desired severity. Challenge routes include aerosolized delivery for respiratory models or intradermal injection for cutaneous reactions. Endpoints are standardized to allow comparison across laboratories: serum IgE titers, airway hyper‑responsiveness (AHR) measured by plethysmography, and lung tissue histopathology.
Longitudinal studies reveal that repeated allergen challenges amplify both IgE levels and eosinophilic recruitment, indicating a progressive escalation of the immune response. Intervention trials targeting Th2 cytokines, IgE binding, or mast‑cell stabilization demonstrate attenuation of early‑phase mediator release and reduction of late‑phase cellular infiltration, confirming the mechanistic relevance of each stage.
In summary, the allergic cascade in rats proceeds from IgE sensitization, through immediate mast‑cell degranulation, to a delayed infiltrative inflammation mediated by eosinophils and cytokines. Precise timing, cellular participants, and measurable biomarkers define each phase, providing a robust framework for investigating therapeutic strategies and for extrapolating findings to human allergic disease.