Related Experiment Video
Updated: Aug 4, 2025
Development of an Economical DNA Delivery System by "Acufection" and its Application to Skin Research
Published on: April 19, 2017
Cytokine transcriptome profiling in acute experimental canine atopic dermatitis skin lesions after IL-31 inhibition
Chie Tamamoto-Mochizuki1, Natalie Crawford2, Jordan M Eder3
1Department of Clinical Sciences, College of Veterinary Medicine, NC State University, Raleigh, North Carolina, USA.
Background:
The caninised monoclonal antibody lokivetmab (LKV), directed at interleukin (IL)-31, is very effective at controlling pruritus in most dogs with atopic dermatitis (AD). However, evidence exists that IL-31 is not required for the induction of acute allergic skin inflammation, which might explain why this treatment is less efficacious in some dogs with AD.
Hypothesis/Objectives:
To compare the comprehensive transcriptome analysis of house dust mite (HDM)-sensitised dogs with and without treatment with LKV to attest our hypothesis that LKV does not majorly affect acute cytokine/chemokine production.
Animals:
Six HDM-sensitised atopic Maltese-beagle dogs.
Materials And Methods:
In this cross-over study, the cytokine profiling of acute AD skin lesions was compared by RNA sequencing (RNA-Seq), with or without LKV-induced inhibition of IL-31. Skin biopsies were obtained from each dog at 0, 6, 12, 24, 48, and 96 h after epicutaneous HDM allergen provocation.
Results:
Macroscopic and microscopic skin lesion scores were not significantly different between the LKV- and nontreatment groups at any time points. Likewise, the results of RNA-Seq analysis revealed no significant difference in the messenger (m)RNA expression of the major cytokines between these two groups. In LKV-treated dogs, IL6, IL9, IL13, IL33, CCL17, and CCL22 were significantly upregulated compared to their baseline expression levels, suggesting that these cytokines are unaffected by IL-31 inhibition.
Conclusions And Clinical Relevance:
IL-31 inhibition is insufficient to prevent the expression of other proinflammatory mediators in acute AD and these could be considered as other potential therapeutic targets.
