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Immunology/Inflammation Laboratory Services

OVA-Induced Allergic Asthma

Commonly Utilized Model Of Airway Inflammation


OVA-Induced Allergic Asthma Efficacy Model

The immune response during asthma is well preserved between mice and humans. In human asthma, eosinophils and lymphocytes are found to infiltrate the bronchial mucosa. Increased mucus secretion and production of Th2 associated cytokines such as IL-4, IL-5 and IL-13 are also found. IL-4 induces differentiation of CD4 T cells into Th2 cells, induces the proliferation of activated B cells and is the major cytokine involved in B cell class switching to IgE (the antibody isotype most associated with human asthma). IL-5 is involved in eosinophil activation and also facilitates B cell growth and antibody production. The activities of IL-13 and IL-4 show a high level of overlap, although it is thought that IL-4 acts primarily in the initial sensitization, with IL-13 more important during secondary exposure to the allergen. In addition to inducing IgE production, IL-13 can induce AHR, goblet cell metaplasia and air- way glycoprotein hyper-secretion, which all contribute to airway obstruction. Mast cells are also central to the development of asthma due to their ability to release an array of preformed and newly synthesized inflammatory mediators such as cytokines, leukotrienes and prostaglandins. 


While we know many factors and events that play an important role in the initiation, progression and persistence of allergic asthma, there is still a lot to be understood about the immuno-regulatory mechanisms. The murine OVA-induced asthma model is a widely used model that results in the characteristic features of asthma allowing the study and assessment of novel treatments.


  • Cell populations in the BALF by FACS
  • Cytokine profile in BALF or lung tissue by multiplex
  • IgE levels
  • Total Protein
  • Histology

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Cytokine Profile in the OVA-induced Asthma Model

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Serum lgE Levels in the OVA-induced Asthma Model

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  • mouse acute model
  • mouse chronic model
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