FITC or DNCB Contact Dermatitis

Contact dermatitis is inflammation of the skin resulting from direct contact with a foreign substance. There are two main types of contact dermatitis: irritant and allergic. Irritant contact dermatitis occurs when the skin comes in contact with a harsh or dangerous substance usually resulting from structural damage to the skin (loss of oils, moisture, and increased permeability). Allergic contact dermatitis which is also known as contact hypersensitivity indicates an overreaction of the body's immune system to a normally harmless substance. Irritant contact dermatitis may occur on first contact with the substance while contact hypersensitivity requires previous sensitisation to the substance to have occurred. Unlike atopic eczema in contact dermatitis this sensitisation almost always occurs via the skin. Clinically allergic contact dermatitis is a common cause of occupational allergic dermatitis and may be caused by a wide variety of substances such as heavy metals i.e. nickel, a variety of petrochemicals, many of which are used in dyes and paints or plant derived compounds. The rash associated with poison oak/ivy exposure is also an example of allergic contact hypersensitivity (urushiol-induced contact dermatitis).

 

In contact hypersensitivity the sensitizing agent is usually a small molecule which alone would be insufficient to generate an immune response however During the sensitisation phase of allergic contact dermatitis these small molecules become immunogenic by binding to proteins within the skin and acting as a hapten. These proteins are then picked up by Langerhans cells of the skin and subsequently present haptenated peptides to T cells in the draining lymph nodes. Subsequent re-exposure results in expansion of these T cells and infiltration of these into the skin where they induce the recruitment of additional cells resulting in the dermatitis.

 

FITC or DNCB induced models of Contact Dermatitis 

During the sensitisation phase skin on the flanks is exposed topically to either FITC or DNCB on two occasions. During this phase of the models these small molecules become immunogenic by binding to proteins within the skin and act as haptens. These haptenated proteins are then picked up by Langerhans cells of the skin and subsequently present haptenated peptides to T cells in the draining lymph nodes. In the challenge phase, mice are then challenged on the ear with the FITC or DNCB. During this phase haptenated peptides are again presented to T cells in the draining lymph nodes, however as the cells are already primed an inflammatory response occurs leading to the development of dermatitis. In the DNCB induced model the inflammation is Th1 mediated (IFN-g, IL-12) also with a role for CD8+ T cells, and macrophage like monocytes. In the FITC induced model is Th2 (IL-4, IL-5) mediated, a role for eosinophils and mast cells has also been demonstrated in this model.
 
These models share many of the features of human contact dermatitis, both sensitization and challenge occurs epicutaneously, during the sensitisation phase no pathology is observed within exposed skin but on subsequent exposure exposed skin becomes red, swollen and hyperplasic, there is also a loss of barrier function in the skin. The distinct sensitisation and challenge phases and the distinct locations of these events allow the modulation of the immune response at either stage. 

Assessments:

  • Ear thickness
  • Circulating or tissue level Biomarker analysis (protein or mRNA)
  • Cell Populations in Spleen/Lymph Node by FACS
  • Histology/IHC
  • PK blood collections

 

SPECIES AVAILABLE:

  • mouse FITC
  • mouse DNCB

 

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