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Hapten-Induced Atopic Dermatitis Model

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Model Introduction

This model induces a skin inflammatory response through repeated, long-term stimulation of experimental animals using haptens (such as Oxazolone, Ox, or Trinitrochlorobenzene, TNCB). The principle is that the hapten initially triggers a typical Th1-cell-mediated delayed-type immune response (similar to delayed-type hypersensitivity, DTH). With increasing frequency of stimulation, the inflammation gradually shifts toward a Th2-cell-mediated chronic inflammation. Because this model covers the evolution from a delayed Th1 response to a chronic allergic response, it is an ideal substitute for studying the mechanisms of DTH and its transformation into chronic allergy.

Research Applications

  1. Exploring the pathogenesis of allergic contact dermatitis.
  2. Studying the pathophysiological process of the immune response shifting from Th1 to Th2.
  3. Screening and evaluating therapeutic drugs for chronic recurrent inflammatory skin diseases.
  4. Assessing the impact of environmental allergens on the skin immune system.

Key Points of Experimental Design

  • Species: Hairless mice (data suggests they exhibit good reactivity under repeated stimulation).
  • Reagents: Oxazolone (Ox) or Trinitrochlorobenzene (TNCB).
  • Method: Repeated, long-term topical application of haptens to the mouse skin.
  • Key Steps:
    1. Select age-appropriate mice and define the administration area.
    2. Perform initial sensitization using a specific concentration of Ox or TNCB.
    3. Conduct repeated stimulations according to the experimental design to induce the transition from acute delayed response to chronic inflammation.
  • Characteristics: High reproducibility, predictability, low cost, and relatively fast modeling speed.

Key Monitoring Indicators

  • Histopathological Observation: Epidermal hyperproliferation, infiltration of lymphocytes, mast cells, and eosinophils in the dermis.
  • Cytokine Detection: High expression of IL-4 in skin tissue.
  • Serological Indicators: Elevated serum IgE levels.
  • Clinical Manifestations: No specific records based on current data.

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