Page 1010 - Veterinary Immunology, 10th Edition

regulates some immune defense genes.
VetBooks.ir cases. The yeast Malassezia pachydermatis produces a phospholipase
Malassezia skin and ear infections are also common in canine AD

that may disrupt skin cell membranes and initiate a secondary

dermatitis either by directly triggering inflammation or by acting as
an allergen. Dogs with atopic dermatitis have higher mRNA
expression of β-defensins in infected, atopic skin, but this may
simply reflect the presence of secondary infections. Environmental

pollution also influences the development of AD (Box 30.3).

Box 30.3

The Aryl Hydrocarbon Receptor and

Atopic Dermatitis

As noted in Box 21.1, the aryl hydrocarbon receptor (AhR) was
originally described by toxicologists investigating the toxicity of
environmental pollutants such as aromatic hydrocarbons and
dioxanes. It has now been shown that there is a direct link between

environmental pollution, the AhR, and the development of atopic
dermatitis (AD).
Thus air pollutants such as diesel exhaust particles bind to the
AhR. The receptor then translocates to the cell nucleus and

upregulates multiple genes. These include the genes encoding IL-
33 and TSLP, both of which trigger pruritus. Additionally, the AhR
upregulates a protein called artemin in keratinocytes. Artemin acts
on peripheral sensory nerves to promote sprouting of peripheral

nerve fibers into the epidermis and upregulates expression of the
capsaicin and wasabi receptors. (Both of these detect chemical
irritants.) Collectively, these changes induce extreme skin
sensitivity. This can explain how allergic individuals develop

“allokinesis”—where mild skin stimulation triggers intense
pruritus.
Interestingly, the endogenous ligands of AhR include products
from the yeast Malassezia as well as from intestinal bacteria such as

lactobacilli and some foods. All have been associated with the
development of AD in pets. Likewise, it is no coincidence that dogs
in households where smoking occurs are significantly more likely
to develop AD than those in non-smoking homes.

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