Difference of Inflammatory Cell Migration in Asthma: A New Hypothesis

Asthma is an inflammatory airway disease and T helper 2 cytokines (i.e., interleukin 4, interleukin 5 [IL-5], and interleukin 13) have an important role in asthma pathology. Blood vessels in lung parenchyma and airway wall serve as the sources for inflammatory cells. The IL-5 leads to eosinophilic inflammation. The adhesion molecules on the endothelium and immune cells allow for the translocation of eosinophils. The vessels of the lung may play the main role in the cell migration and pathophysiology of asthma.

Several keywords were searched in databases, and out of 495 manuscripts 178 studies were selected. At least, 19 manuscripts were used as support of the above-mentioned hypothesis.

We hypothesized that airway vessels highly have leaks for eosinophils, and eosinophil migration from the endothelium of these vessels is easier than the endothelium of other tissues. Severe vascular leak and easy eosinophil migration in lung vessels cause inflammation leading to severe asthma phenotype; however, similar inflammation does not occur in other organs. The treatment of asthma is difficult and the control of cell migration needs to manipulate cell adhesion molecules.

The lung endothelial molecules may have the potential to develop new treatments for asthma.