The pathophysiologic mechanism of allergic asthma and rhinosinusitis is so complicated and involves thousands of inflammatory mediators. They are world-wide health problems, with their steadily increasing prevalence and their negative impact on quality of life. In spite of many studies throughout the world, there are still many more pathophysiologic mechanisms to be uncovered and current mainstream of medication still remains for symptom control including bronchodilators such as β2 agonists, inhaled and systemic corticosteroid, antihistamines, and leukotriene modifiers, all only with transient symptomatic relief. Therefore, we should focus on novel mechanism and mediators so that we could better understand and cure allergic asthma and rhinosinusitis.

There are a number of topics related to pathophysiologic mechanisms. For example, we could focus on innate immunity (such as Toll-like receptors) and humoral immunity (such as immunoglobulins, cytokines, and chemokines). We could also study genetic change, upregulation or suppression of some specific genes, and their correlation with phenotypes.

If you are performing researches about these or similar topics about allergic asthma and/or rhinosinusitis, publishing your result and communicating your opinion through Mediators of Inflammation could be a great chance to announce your valuable work.

Therefore, we cordially invite you to contribute original research articles as well as review articles that will elucidate the pathophysiologic mechanisms and potential mediators related with allergic asthma and rhinosinusitis through laboratory and/or clinical studies using cell lines, laboratory animals, and human beings.

Potential topics include but are not limited to the following:

• Innate immunity associated with allergic asthma and rhinosinusitis
• Cytokines and chemokines associated with allergic asthma and rhinosinusitis
• Laboratory/clinical studies to elucidate pathophysiologic mechanisms
• Genetic variation and/or mutation associated with pathophysiology
• Therapeutic effect and mechanism of new, novel agents