Renz Harald, Kiliç Ayşe
Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University Marburg, Marburg, Germany.
Chem Immunol Allergy. 2012;98:100-17. doi: 10.1159/000336504. Epub 2012 Jun 26.
Allergic asthma is a chronic inflammatory disease characterized by the production of allergen-specific IgE antibodies, TH2 inflammation, airway hyperresponsiveness and airway remodeling. Airway remodeling represents the disease-limiting stage during disease progression, and the underlying cellular molecular network resulting in airway remodeling are still poorly defined. In addition to the well-established TH2-dependent inflammatory response, several lines of investigation reveal that this regulation in the peripheral central nervous system contributes to disease development, exacerbation and progression. Several members of the neurotrophin family (e.g. nerve growth factor, brain-derived neurotrophic factor) are important transmitters of signals between the immune and the nervous system. Recent data indicate that NGF contributes to the development of airway remodeling in an inflammation and TGF-independent manner. These and other data open the opportunity to therapeutically interfere also on this level of regulation as a novel approach.
过敏性哮喘是一种慢性炎症性疾病,其特征为产生过敏原特异性IgE抗体、TH2炎症、气道高反应性和气道重塑。气道重塑是疾病进展过程中的疾病限制阶段,导致气道重塑的潜在细胞分子网络仍未明确界定。除了已确定的TH2依赖性炎症反应外,多项研究表明,外周中枢神经系统中的这种调节作用有助于疾病的发生、加重和进展。神经营养因子家族的几个成员(如神经生长因子、脑源性神经营养因子)是免疫和神经系统之间信号的重要传递者。最近的数据表明,NGF以一种不依赖炎症和转化生长因子的方式促进气道重塑的发展。这些数据以及其他数据为作为一种新方法在这一调节水平上进行治疗干预提供了机会。