Abstract
Asthma increases worldwide without any definite reason and patient numbers double every 10 years. Drugs used for asthma therapy relax the muscles and reduce inflammation, but none of them inhibited airway wall remodeling in clinical studies. Airway wall remodeling can either be induced through pro-inflammatory cytokines released by immune cells, or direct binding of IgE to smooth muscle cells, or non-immunological stimuli. Increasing evidence suggests that airway wall remodeling is initiated early in life by epigenetic events that lead to cell type specific pathologies, and modulate the interaction between epithelial and sub-epithelial cells. Animal models are only available for remodeling in allergic asthma, but none for non-allergic asthma. In human asthma, the mechanisms leading to airway wall remodeling are not well understood. In order to improve the understanding of this asthma pathology, the definition of “remodeling” needs to be better specified as it summarizes a wide range of tissue structural changes. Second, it needs to be assessed if specific remodeling patterns occur in specific asthma pheno- or endo-types. Third, the interaction of the immune cells with tissue forming cells needs to be assessed in both directions; e.g., do immune cells always stimulate tissue cells or are inflamed tissue cells calling immune cells to the rescue? This review aims to provide an overview on immunologic and non-immunologic mechanisms controlling airway wall remodeling in asthma.
Highlights
The prevalence of asthma has been increasing worldwide for at least three decades, without any definite reason
The mechanism(s) by which air pollution alters the structure of the lung tissues is not well understood, but it was suggested that the interaction between the environment and epigenetic events plays a major role in the pathogenesis of asthma [13]
It should be considered that airway wall remodeling caused the increased expression of type-2-cytokines by human airway epithelial cells [31]. These findings indicate that bi-directional crosstalk between tissue forming cells and immune cells exists, and plays an important role in the pathogenesis of asthma
Summary
The prevalence of asthma has been increasing worldwide for at least three decades, without any definite reason. The mechanism(s) by which air pollution alters the structure of the lung tissues is not well understood, but it was suggested that the interaction between the environment and epigenetic events plays a major role in the pathogenesis of asthma [13]. Many studies reported that the different asthma phenotypes, which were described based on patient symptoms, could not be well separated by specific cellular pathologies [18,19,20]. These findings suggest that the pathogenesis of asthma must be re-evaluated, by not focusing solely on the immune response
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