How Does Atopic Dermatitis Affect the Skin and Body?

Atopic dermatitis, or atopic eczema, affects the skin, causing itchiness, dryness, scaly patches, or weepy, blistering patches. To understand how atopic dermatitis (AD) affects the skin, it’s important to review the purpose and structure of the skin.1

Skin layers and function

The skin is the largest and fastest-growing organ in the body. The skin has several important functions, including:

  • To hold in the organs, muscles, and other tissues
  • To maintain the body’s temperature
  • To protect the internal structures from germs and water2

The skin is made up of several layers, each providing a role in the protection of the body:

  • Epidermis: The epidermis is the outermost layer of the skin and is made up of several layers of cells. The epidermis can be further subclassified into 4 layers: the stratum corneum or corneal layer, the granular cell layer, the spinous or prickle-cell layer, and the basal layer. The corneal layer is the visible part of the skin and protects the body from germs. The granular layer is noted by the transition of cells becoming more flattened and its cells secrete important substances that help to keep our epidermal barrier intact. The spinous layer plays a significant role in the immune responses of the skin, and the basal layer continually renews the skin by growing new cells.
  • Dermis: The dermis is the middle layer. The dermis is responsible for making sweat to cool the body, containing the nerve endings that enable the sense of touch, housing the hair follicles, making oil to moisturize and make the skin waterproof, and enclosing the blood vessels that provide food and waste removal for the skin.
  • Subcutaneous fat layer: The inner or deepest layer is the subcutaneous fat layer. This layer contains fat that helps in the temperature regulation of the body. The subcutaneous layer also attaches the dermis to the muscles and bones.2-4

How atopic dermatitis affects the skin

The corneal layer of the skin contains a protein called filaggrin, which plays a key role in the corneal layer’s structure and formation. In some people with AD, there can be a partial or complete lack of filaggrin, due to mutations in the FLG gene. Researchers have identified more than 40 mutations in FLG that have been associated with up to 50% of patients with moderate to severe AD.

These genetic mutations cause a lack of filaggrin in the corneal layer, which leads to a reduced ability to maintain the skin’s natural amount of water. Excess water loss can lead to dry skin, which then causes itchiness. The lack of filaggrin may also allow for the entry of airborne allergens to enter the skin, which could lead to an inflammatory response by the immune system.

Atopic Dermatitis

Another theory suggests that the normal pH of the skin barrier may be affected by filaggrin defects, which could lead to the overgrowth of bacteria. This could then trigger the immune system to create inflammatory skin lesions. However, not all individuals who have FLG mutations develop AD, and not all patients with AD have mutations is FLG. While FLG is one of the first identified and most well-studied genes associated with AD, there are many other genes that likely play a role in the development of AD. This is an active area of investigation for researchers.5

An abnormal immune system response also plays a role in the development of AD. Several cytokines (chemical messengers) are overly abundant in AD, causing an overload of T-cells (a type of white blood cell) to come to the skin. Specifically, abnormal numbers of T-helper cell 2 (Th2) are brought to the skin in AD, causing inflammation.6

Emily Downward | June 2017
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