Turner Lab

The research laboratory of Matthew Turner, MD, PhD, focuses on the interaction between skin injury, inflammation and wound healing. These interactions are important for inflammatory skin diseases such as atopic dermatitis (atopic eczema) and conditions that impair the wound healing, such as diabetes mellitus. The goal of the Turner Lab is to discover new molecular pathways that promote inflammatory skin diseases and impair wound healing and translate these discoveries into improved novel treatments for patients.

The Turner Lab studies mechanisms of skin inflammation that contribute to atopic dermatitis (AD), one of the most common inflammatory diseases in humans and one that disproportionately affects children (up to 1 in 5 children). Atopic dermatitis is associated with significant morbidity due to severe itching, poor sleep and secondary skin infections—all of which can dramatically impair quality of life and productivity for patients and their caregivers. Treatment options for atopic dermatitis are limited and often ineffective. A better understanding of the mechanisms that cause and perpetuate atopic dermatitis is needed in order to identify new cellular and molecular targets for therapy. The Turner Lab is contributing to the understanding of the causes of atopic dermatitis through research with vitro systems, mouse models of atopic dermatitis and healthy and diseased human subjects.

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Active Research

A major focus of the Turner Lab is investigating inflammatory mediators (cytokines) produced by skin cells (keratinocytes) and immune cells (e.g. T cells and basophils) in order to understand the production, cellular targets and effects of these cytokines in atopic dermatitis. The cytokine interleukin 33 (IL-33) can be produced by keratinocytes, other epithelial cell types and a variety of immune cells populations.

In studying the Stat6VT mouse model of atopic dermatitis, the Turner Lab discovered IL-33 levels are increased in diseased skin. Subsequent studies with Stat6VT mice that are genetically deficient for IL-33 demonstrated increased disease severity, which suggests IL-33 has a protective role against atopic dermatitis-like disease in this model. The Turner Lab is investigating the mechanism underlying this observation. The Turner Lab has also played an important role in demonstrating the AD-like phenotype in Stat6VT mice parallels many aspects of human disease suggesting this is an excellent preclinical model in which to discover new disease targets and perform preclinical testing of potential therapeutics.

Mechanical injury to the skin is thought to contribute to the initiation, progression and/or persistence of a number of inflammatory skin diseases such as atopic dermatitis and psoriasis. For example, IL-33 (mentioned above) is released from keratinocytes in response to mechanical injury to the skin. In fact, keratinocytes produce and store several preformed inflammatory mediators under normal conditions; these include the cytokines IL-33 and HMGB1. These cytokines are grouped into a larger class of molecules called alarmins. Alarmins are released by injured cells to trigger inflammation that can protect the host against acute infection of injured tissue in the short term and promote adaptive immune responses (e.g. in the case of vaccination) to protect against future threats of infection in the long term.

The Turner Lab is currently studying the sterile inflammatory responses that are triggered by mechanical injury to the skin and investigating the role of alarmins in regulating these responses. In addition to understanding the roles of skin injury in inflammatory diseases such as atopic dermatitis and psoriasis, the Turner Lab is investigating the contribution of these injury-induced inflammatory cascades to disorders in which wound healing is impaired as in patients with diabetes mellitus.

By defining the mechanisms that regulate skin-injury induced inflammation, the Turner Lab seeks to parse out the beneficial aspects of inflammation from the detrimental aspects of inflammation in regards to wound healing and then design new treatments that promote wound healing in patients with diabetes and a host of other diseases.

Research Funding

Role of keratinocyte-derived cytokines in epidermal injury and atopic dermatitis
Goals: Define mechanisms by which IL-33 regulates AD-like disease in Stat6VT mice.

Platelet-activating factor and Epidermal Cytotoxicity

Goals: Determine how short-term ethanol exposure augments production of platelet-activating

factor following thermal burn- or ultraviolet B radiation-induced skin injury.

Recent Publications

For a full list of publications, find Matthew Turner, PhD, on PubMed.

DaSilva-Arnold SC, Thyagarajan A, Seymour LJ, Yi Q, Bradish JR, Al-Hassani M, Zhou H, Perdue, NJ, Nemeth V, Krbanjevic A, Serezani APM, Olson MR, Spandau DF, Travers JB, Kaplan MH, Turner MJ. Phenotyping acute and chronic atopic dermatitis-like lesions in Stat6VT mice identifies a role for IL-33 in disease pathogenesis. Arch Dermatol Res. 2018 Apr;310(3):197-207. PubMed PMID: 29368135.

Krishnamurthy P, Da-Silva-Arnold S, Turner MJ, Travers JB, Kaplan MH. Poly-ADP ribose polymerase-14 limits severity of allergic skin disease. Immunology. 2017 Nov;152(3):451-461. PubMed PMID: 28653395; PubMed Central PMCID: PMC5629435

Serezani AP, Bozdogan G, Sehra S, Walsh D, Krishnamurthy P, Sierra Potchanant EA, Nalepa G, Goenka S, Turner MJ, Spandau DF, Kaplan. MH. IL-4 impairs wound healing potential in the skin by repressing fibronectin expression. J Allergy Clin Immunol. 2017 Jan;139(1):142-151.e5. PubMed PMID: 27554818; NIHMSID: NIHMS811653; PubMed Central PMCID: PMC5222746.

Sehra S, Krishnamurthy P, Koh B, Zhou HM, Seymour L, Akhtar N, Travers JB, Turner MJ, Kaplan MH. Increased Th2 activity and diminished skin barrier function cooperate in allergic skin inflammation. Eur J Immunol. 2016 Nov;46(11):2609-2613. PubMed PMID: 27510401; NIHMSID: NIHMS832933; PubMed Central PMCID: PMC5142240.

Turner M, DaSilva-Arnold S, West C, Sun L, Hall C, Bradish J, Kaplan M, Travers J, and Y Sun. 2014. Stat6 Mediated Keratitis and Blepharitis: a Novel Murine Model of Ocular Atopic Dermatitis. IOVS. 55:3803.