Intracellular Signalling

Inflammatory lung diseases such as asthma, sarcoidosis and chronic obstructive pulmonary disease (COPD) are common diseases contributing high costs for the society and there is a need for novel innovative treatments, especially for COPD as no currently available drug therapy reduces the relentless progression of this severe disease.

To provide a basis for the development of new therapeutic strategies, we are undertaking a translatory research approach linking basic mechanistic studies with clinical research to increase the molecular understanding of inflammatory lung diseases.

Our studies are centered around mechanisms inside the cell that controls inflammatory processes and cellular differentiation, with a focus on regulation of gene expression. We use advanced cell and molecular biology methods to study lung cells from the sick patient obtained via bronchoscopy, allowing us to directly study the diseased organ. We combine these studies with generation and analysis of gene targeted mouse models, and mechanistic studies in in vitro cell models.

Previous studies

Intracellular Signalling Mechanisms in Inflammatory Lung Diseases

During the last years we have established a previously unknown role for a group of transcription factors called C/EBPs in the regulation of gene expression in lung (Nord et al, 1998; Cassel et al, 2000; Cassel et al, 2002). Subsequently, we have found that C/EBPs have a role in mediating the effects of corticosteroids in lung, hormones that have a central role in the treatment of inflammatory lung diseases, especially asthma (Berg et al, 2002; Berg et al, 2005). We have recently made the seminal finding that C/EBP-activity is increased in the lungs of healthy smokers, whereas smokers that develop COPD lack this increase (Didon et al, 2005). This inability to activate C/EBPs could play a role in the pathogenesis of COPD, as C/EBPs are known to activate many genes involved in defense mechanisms, including anti-oxidative genes and genes within the innate immune system, genes all considered to have a role in the pathogenesis of COPD. The decreased C/EBP-activity in COPD could also help explain the relative resistance to corticosteroid-treatment that characterizes this disease.

Adjunct professor

Magnus Nord


Ongoing studies

Drug Transporters and Metabolising Enzymes in Lung - Impact on Lung PharmacoKinetics and Drug-Drug Interactions in Healthy Subjects and COPD Patients

Procurement officer

Tove Berg

Organizational unit: Integrated Cardio Metabolic Centre