It is no secret that direct contact with poison ivy causes
an uncomfortable agonizing itch. How this happens is still not clearly defined.
As reported in ACS News online, Sven-Eric Jordt of Duke university pinpointed a molecular pathway that helps
transmit an itch signal through nerve cells by exposing mice to poison ivy’s
oily allergen urushiol. Two commonly prescribed drugs to fight the poison ivy
itch are antihistamines and corticosteroids. Unfortunately antihistamines seem
to not work and although corticosteroids fight inflammation they are
ineffective against itch. Jordt looked
for genes that were transcribed at higher levels in mice whose skin was brushed
with urushiol compounds compared to non-exposed mice.
As expected several genes
associated with inflammation were up regulated in the infected mice, but Jordt
focused on one particular gene that codes for the protein interleukin-33,
associated with itchy skin. When the exposed mice were given antibodies against
IL-33, the mice slowed their scratching significantly. When exposed mice were given
antibodies against IL-33’s receptor, ST2, which is located on sensory neurons
that connect to the animals’ skin, also significantly reduced itching. Researchers suspected a link such as this one
but did not know the specifics. Even though a molecular pathway for itch is
complicated, these systems will share features important for future drug
design. Jordt’s team hopes to work with clinicians to see if they can detect
IL-33 in humans with poison ivy.
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