Asthma is a chronic inflammatory disease of the airways. The chronic inflammation causes the airways to swell, which makes them highly sensitive and narrow. Swelling may occur randomly or after exposure to triggers like allergies, smoke, air pollution, and exercise. The main symptoms are wheezing, breathlessness, and coughing that can temporarily worsen and give asthma attacks.

How many have asthma?
Asthma is one of the most prevalent chronic diseases, with more than 300 million affected worldwide. Asthma affects people of all ages and is often starts during childhood, although it also can be developed for the first time in adults. 

How is asthma treated?
The symptoms during asthma can usually be controlled with the treatment of reliever or preventer inhalers. But patients who have severe asthma can have ongoing problems and difficulties controlling their asthma symptoms with treatment causing the risk of asthma attacks.

How is asthma diagnosed?
The current diagnosis of asthma is based on a variably expiratory airflow limitation measured by forced expiratory volume in 1 second (FEV1), family history, and symptoms.

The medical need for biomarkers in asthma is to enable precision medicine. First, a diagnostic biomarker identifying distinct subtypes would be of value due to the heterogenicity entity of the disease. Identification of subtypes would also allow better stratification of patients entering clinical trials. Second, a predictive biomarker to select patients likely to respond to a therapeutic drug in clinical trials may reduce trial length and size required to determine therapeutic efficacy.

The chronic inflammation and swelling of the airways during asthma cause a restructuring of the component of the airway wall, including alteration of the extracellular matrix (ECM). A normal repair response creates a balance between extracellular matrix (ECM) proteins that are broken down and rebuilt, but this is disturbed during chronic inflammation. The altered balance leads to a distinct tissue turnover in asthma that can be quantified by protein fingerprint biomarkers in a serological sample.

While the asthma field possesses several diagnostic biomarkers subtyping asthma patients, their capacity for predicting treatment response is limited. Therefore, there is still a medical need for biomarkers that can predict treatment response. This may be achieved by the characterization of structural changes in the tissue and linking it to a specific subtype of asthma. The Protein Fingerprint biomarkers can be measured in serum and used to accurately quantify changes in tissue remodeling in the individual patient.


Protein Fingerprint biomarkers measured in serum are generally increased in asthma patients compared to healthy individuals and correlate with airway resistance.


ECM remodelling quantified by MMP degraded type I (C1M), type IV (C4M2), and the lung specific type IV (C4Ma3) collagen are all increased in asthmatic patients compared to healthy controls.

Protein Fingerprint biomarkers measured in serum are associated with subtypes of asthma.


Lung tissue degradation quantified by MMP degraded collagen type IV α3 chain (C4Ma3) is increased in asthmatic patients with high eosinophil count and asthmatics patients with a high type 2 cytokine profile.

Protein Fingerprint biomarkers measured in serum are associated with exacerbations in asthmatic patients.


Lung tissue degradation quantified by MMP degraded collagen type IV (C4M2), and collagen type IV α3 chain (C4Ma3) are increased in asthmatics experiencing exacerbations.

Protein Fingerprint biomarkers are predictive of clinical response by being increased in responders as compared to non-responders at baseline. Effective treatments further suppress the Protein Fingerprint biomarkers.


Lung tissue degradation quantified by MMP degraded collagen type IV α3 chain (C4Ma3) is increased in responders compared to non-responders at baseline.

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