The role of microbial influence on atopic eczema and inflammatory skin diseases – from molecular mechanisms to therapy.

Project: Research

Research areas and keywords

UKÄ subject classification

  • Dermatology and Venereal Diseases


The general aim of the research-project is to generate new understanding of the microbial influence on inflammatory skin disease and to explore mechanisms involved in microbial impact on the skin contra host defense and inflammation. Moreover, the project aims to develop novel strategies for prevention and treatment of inflammatory skin diseases.

Atopic eczema is characterized by chronic inflammation, dysfunction of the skin barrier and defects in innate immunity, and this balance is disturbed resulting in cutaneous colonization of microbial pathogens which will maintain the inflammatory response. Several pro-inflammatory cytokines and other molecules are candidates for discovery of new disease severity markers in atopic eczema.

Microbial pathogens and their products play an influential role and are potential triggers for the maintenance of the inflammatory processes in skin diseases such as atopic eczema. Specifically, the project may lead to new understanding of the role of Staphylococcus aureus and other skin-associated microbial pathogens in the pathogenesis of atopic eczema. Knowledge of interactions between components of host defense and microbial pathogens can potentially facilitate development of strategies to control the microbial impact in skin infection and inflammation.


1. A. Sonesson et al. Thymic stromal lymphopoietin exerts antimicrobial activities. Exp Dermatol. 2011 Dec;20(12):1004-10.

2. A. Sonesson et al. Sensitization to skin-associated microorganisms in adult patients with atopic dermatitis is of importance for disease severity. Acta Derm Venereol 2013 May;93(3):340-5.

3. C. Ling Jinnestål et al. Skin barrier impairment correlates with cutaneous Staphylococcus aureus colonization and sensitization to skin-associated microbial antigens in adult patients with atopic dermatitis. Int J Dermatol. 2014 Jan; 53(1):27-33.
StatusNot started


  • Sonesson, Andreas (PI)