Abstract

The fibroblast growth factor 2 (FGF2) is a potent mitogenic factor belonging to the FGF family. It plays a role in airway remodeling associated with chronic inflammatory airway diseases, including asthma and chronic obstructive pulmonary disease (COPD). Recently, research interest has been raised in the immunomodulatory function of FGF2 in asthma and COPD, through its involvement in not only the regulation of inflammatory cells but also its participation as a mediator between immune cells and airway structural cells. Herein, this review provides the current knowledge on the biology of FGF2, its expression pattern in asthma and COPD patients, and its role as an immunomodulatory factor. The potential that FGF2 is involved in regulating inflammation indicates that FGF2 could be a therapeutic target for chronic inflammatory diseases.

Highlights

  • Chronic inflammatory airways disease is a major economic burden and public health challenge worldwide

  • In addition to TGF-β, the inflammatory cytokines including IL-4, IL-13, and IL-17, the pivotal mediators driving the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD), enhance fibroblast growth factor 2 (FGF2)-mediated airway smooth muscle cells (ASMCs)’ proliferation in different experiment settings (Bosse et al, 2008; Ogawa et al, 2018), which further support the interaction of FGF2 with inflammation on tissue remodeling in disease status

  • The eotaxin mRNA was shown to be increased in endothelial cells (ECs) from asthma patients, and the level was associated with airway hyperresponsiveness (Ying et al, 1997), which further supports the role of ECs in modulating airway inflammation in chronic inflammatory diseases such as asthma and COPD

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Summary

Introduction

Chronic inflammatory airways disease is a major economic burden and public health challenge worldwide. These data suggest that FGF2 expression is elevated in multiple pulmonary cell types in asthma and COPD, and may be involved in the pathogenesis of chronic inflammatory airway diseases.

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Conclusion
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