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Sirtuin 2 Enhances Allergic Asthmatic Inflammation

Sirtuin 2 Enhances Allergic Asthmatic Inflammation

Yong Gyu Lee, Brenda F Reader, Derrick Herman, Adam Streicher, Joshua A Englert, Mathias Ziegler, Sangwoon Chung, Manjula Karpurapu, Gye Young Park, John W Christman, Megan N Ballinger

JCI Insight. 2019 Feb 21;4(4):e124710.

PMID: 30668546

Abstract:

Allergic eosinophilic asthma is a chronic condition causing airway remodeling resulting in lung dysfunction. We observed that expression of sirtuin 2 (Sirt2), a histone deacetylase, regulates the recruitment of eosinophils after sensitization and challenge with a triple antigen: dust mite, ragweed, and Aspergillus fumigatus (DRA). Our data demonstrate that IL-4 regulates the expression of Sirt2 isoform 3/5. Pharmacological inhibition of Sirt2 by AGK2 resulted in diminished cellular recruitment, decreased CCL17/TARC, and reduced goblet cell hyperplasia. YM1 and Fizz1 expression was reduced in AGK2-treated, IL-4-stimulated lung macrophages in vitro as well as in lung macrophages from AGK2-DRA-challenged mice. Conversely, overexpression of Sirt2 resulted in increased cellular recruitment, CCL17 production, and goblet cell hyperplasia following DRA challenge. Sirt2 isoform 3/5 was upregulated in primary human alveolar macrophages following IL-4 and AGK2 treatment, which resulted in reduced CCL17 and markers of alternative activation. These gain-of-function and loss-of-function studies indicate that Sirt2 could be developed as a treatment for eosinophilic asthma.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP304896284-A	AGK2		304896-28-4	Price

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