Allergic Inflammation Model
Allergic Inflammation Model - Related Videos
07:52
Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
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Cited by 1 •
2012
We describe a strategy to monitor maturation and migration of pulmonary dendritic cells in response to ovalbumin in the setting of ovalbumin induced allergic airway inflammation. This strategy can be modified to assess migration of pulmonary dendritic cells in settings of infection.
02:06
Allergic Reactions
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2019
Overview We speak of an allergy when the immune system triggers a response against a benign foreign structure, like food, pollen or pet dander. These elicitors are called allergens. If the immune system of a hypersensitive individual was primed against a specific allergen, it will trigger allergic symptoms during every subsequent encounter of the allergen. Symptoms can be mild, such as hay fever, to severe, such as potentially fatal anaphylactic shock. Sensitization Is the First Step of an...
08:02
Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
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Cited by 11 •
2015
Although Candida infection models are available to study host immune resistance, a model to study T cell mediated immunopathology in the context of Candida infection is absent. Here we describe a method to establish Th17 immunopathology associated with oral Candida infection in immunodeficient mice.
03:06
A Method to Induce Ocular Surface Inflammation in a Murine Model
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2025
This video demonstrates a method to induce ocular surface inflammation and meibomian gland dysfunction in a murine model. Stimulation of the mouse's immune system using an immunogen and later restimulation with the same immunogen promotes ocular surface inflammation, which causes plugging of meibomian gland secretion through neutrophil-produced aggNETs and leads to dry eye disease.
08:43
Investigating Intestinal Inflammation in DSS-induced Model of IBD
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Cited by 607 •
2012
Experimental models of inflammatory bowel disease have allowed us to examine the complex innate and adaptive immune responses associated with pathogenesis. Using histological scoring, quantification of pro-inflammatory cytokines and myeloperoxidase activity, one can begin to assess these responses seen in inflammatory bowel disease.
FAQs
Allergic inflammation models typically separate immune priming from the inflammatory challenge. During sensitization, exposure to an allergen promotes production of allergen-specific IgE. A later exposure to the same or relevant allergen enables that IgE to participate in mast-cell activation, producing a measurable transition from immune recognition to tissue inflammation. This sequence helps investigators examine disease initiation and amplification.
FcεRI cross-linking is the immediate mast-cell activation step after allergen-specific IgE has been generated. It triggers release of histamine and other mediators, which contribute to the early inflammatory response. The resulting signals also recruit eosinophils, linking an initial receptor-level event to broader cellular infiltration and sustained tissue inflammation. This connection makes FcεRI activity a useful mechanistic focus in model interpretation.
The experimental setting changes what the model can reveal. Cellular systems can focus on interactions among immune components, whereas animal or tissue-based systems can capture broader airway or tissue changes. Selecting among these formats therefore depends on the question being asked, such as examining immune-cell behavior, reproducing disease-associated tissue inflammation, or evaluating how a treatment changes the response.
Eosinophil recruitment is more than a secondary measurement: it indicates that mediator release has progressed into a broader inflammatory response. Measuring this infiltration alongside cytokine production and tissue changes allows researchers to relate cellular accumulation to inflammatory intensity. That combination can help distinguish a model with only an initiating immune signal from one showing amplified tissue-level disease features.
A typical workflow begins by sensitizing the experimental system to an allergen, followed by a subsequent allergen exposure that challenges the primed response. Investigators then assess the resulting inflammation through immune-cell infiltration, cytokine production, and airway or tissue changes. The sequence connects experimental exposure to measurable outcomes and provides a basis for comparing responses with and without an intervention.
Relevant readouts can cover both immune activity and tissue consequences. Immunoglobulin E and cytokine production provide information about allergen-directed and inflammatory signaling, while eosinophil infiltration shows cellular recruitment. Airway or tissue changes add an anatomical outcome, and treatment responses indicate whether an intervention alters the modeled inflammatory process. Together, these measures give a multidimensional assessment rather than a single endpoint.
Allergic inflammation models are useful when researchers need to connect disease mechanisms with therapeutic testing. A study can examine how an intervention affects immune-cell infiltration, cytokine production, airway or tissue changes, or the overall treatment response. This supports evaluation of anti-inflammatory and antiallergic therapies in experimental representations of asthma, dermatitis, or allergic rhinitis.
In medicine-focused research, the model helps compare inflammatory patterns across different allergic conditions while preserving a common immune framework. Airway-oriented changes can support asthma-related studies, whereas tissue inflammation can inform dermatitis or allergic-rhinitis investigations. Because the systems may be cellular, animal, or tissue-based, researchers can match the experimental format to the disease feature and outcome they need to study.