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Mediators of Inflammation
Volume 2015 (2015), Article ID 879783, 8 pages
http://dx.doi.org/10.1155/2015/879783
Review Article

Cellular Mechanisms Underlying Eosinophilic and Neutrophilic Airway Inflammation in Asthma

1Department of Medical and Surgical Sciences, University “Magna Græcia” of Catanzaro, Viale Europa, Località Germaneto, 88100 Catanzaro, Italy
2Department of Medicine and Surgery, University of Salerno, Via Salvador Allende, Baronissi, 84081 Salerno, Italy
3Department of Health Science, University “Magna Græcia” of Catanzaro, Viale Europa, Località Germaneto, 88100 Catanzaro, Italy
4Department of Cardiothoracic and Respiratory Sciences, 2nd University of Naples, Via Leonardo Bianchi, 80131 Naples, Italy

Received 13 January 2015; Accepted 23 February 2015

Academic Editor: Helen C. Steel

Copyright © 2015 Girolamo Pelaia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Asthma is a phenotypically heterogeneous chronic disease of the airways, characterized by either predominant eosinophilic or neutrophilic, or even mixed eosinophilic/neutrophilic inflammatory patterns. Eosinophilic inflammation can be associated with the whole spectrum of asthma severity, ranging from mild-to-moderate to severe uncontrolled disease, whereas neutrophilic inflammation occurs mostly in more severe asthma. Eosinophilic asthma includes either allergic or nonallergic phenotypes underlying immune responses mediated by T helper (Th)2 cell-derived cytokines, whilst neutrophilic asthma is mostly dependent on Th17 cell-induced mechanisms. These immune-inflammatory profiles develop as a consequence of a functional impairment of T regulatory (Treg) lymphocytes, which promotes the activation of dendritic cells directing the differentiation of distinct Th cell subsets. The recent advances in the knowledge of the cellular and molecular mechanisms underlying asthmatic inflammation are contributing to the identification of novel therapeutic targets, potentially suitable for the implementation of future improvements in antiasthma pharmacologic treatments.