Chronic Inflammation

We are interested in the pathogenesis of chronic inflammation, especially the type 2 inflammation that is associated with allergic diseases such as asthma, atopic dermatitis, and eosinophilic esophagitis. Type 2 inflammation is characterized by the accumulation of eosinophils, mast cells and M2 macrophages in tissues. It is typically driven by Th2 lymphocytes and associated with an increase of IgE antibodies, but recent studies have demonstrated that innate lymphoid cells also contribute and sometimes are the main instigators of type 2 inflammation. Our research focuses on a mouse mutant that lacks a protein called SHARPIN. These chronic proliferative dermatitis (cpdm) mice were discovered by us in the early 1990’s. The mice have a complex phenotype with immune system defects, dermatitis and systemic inflammatory disease. In collaboration with John Sundberg at the Jackson Laboratory (Bar Harbor, Maine), we mapped the mutation to the Sharpin gene. Ongoing studies are aimed at understanding the mechanism by which absence of SHARPIN leads to inflammation. SHARPIN is a component of the linear ubiquitin assembly complex (LUBAC) together with the proteins HOIP and HOIL1. This complex adds ubiquitin molecules via Met1 linkages to IKKγ (a.k.a. NEMO) which is required for proper functioning of the canonical NFkB signaling pathway. In the absence of SHARPIN, the mice develop a progressive chronic dermatitis with histologic features of atopic dermatitis and an eosinophilic esophagitis at about 4-5 weeks of age. The dermatitis and esophagitis develop in the absence of B and T lymphocytes.

Esophagus
Mast Cells

Selected publications

Contact Information

The HogenEsch Lab
725 Harrison Street
West Lafayette, IN 47907
USA
e-mail: hogenesch@purdue.edu
phone: 765-496-3487

Purdue University College of Veterinary Medicine, 625 Harrison Street, West Lafayette, IN 47907, (765) 494-7607

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