Bronchial asthma is caused by allergic airway inflammation, resulting in reversible airway obstruction, characterized by airway hyper-responsiveness, bronchoconstriction, increased mucus secretion and an increase in lung vessel permeability.

The pathophysiological changes in asthma have been attributed to the altered expression of biologically plausible proteins associated with transcriptional pathways, inflammatory mediators, chemokines, cytokines, apoptosis and cell proliferation. Such multifactorial diseases characteristically involve an interplay of many genetic variations of molecular and biochemical pathways and their interactions with environmental factors. The complex nature of the asthma phenotype, together with genetic heterogeneity and environmental influences, has made it difficult to uncover the aspects that underlie this common disease. Recently, genomic and proteomic technologies have been developed to identify associations between genes, proteins and disease. This approach, called 'omics biology', aims to recognize early onset of disease, institute preventive treatment and identify new molecular targets for novel drugs in multifactorial diseases. This article reviews examples of how proteomic technology can be used to find asthma marker proteins (from the cell model to clinical samples).

Identification of protein changes in different stages of asthma could provide further insights into the complex molecular mechanisms involved in this disease. These studies provide new insights for finding novel pathological mediators and biomarkers of asthma.