College of Engineering, University of Georgia, Athens, GA, USA.
Department of Mathematics and Statistics, San Diego State University, San Diego, CA, USA.
Inflamm Res. 2019 Jan;68(1):59-74. doi: 10.1007/s00011-018-1191-2. Epub 2018 Oct 10.
Inflammation in the lung is the body's natural response to injury. It acts to remove harmful stimuli such as pathogens, irritants, and damaged cells and initiate the healing process. Acute and chronic pulmonary inflammation are seen in different respiratory diseases such as; acute respiratory distress syndrome, chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis (CF).
In this review, we found that inflammatory response in COPD is determined by the activation of epithelial cells and macrophages in the respiratory tract. Epithelial cells and macrophages discharge transforming growth factor-β (TGF-β), which trigger fibroblast proliferation and tissue remodeling. Asthma leads to airway hyper-responsiveness, obstruction, mucus hyper-production, and airway-wall remodeling. Cytokines, allergens, chemokines, and infectious agents are the main stimuli that activate signaling pathways in epithelial cells in asthma. Mutation of the CF transmembrane conductance regulator (CFTR) gene results in CF. Mutations in CFTR influence the lung epithelial innate immune function that leads to exaggerated and ineffective airway inflammation that fails to abolish pulmonary pathogens. We present mechanistic computational models (based on ordinary differential equations, partial differential equations and agent-based models) that have been applied in studying the complex physiological and pathological mechanisms of chronic inflammation in different airway diseases.
The scope of the present review is to explore the inflammatory mechanism in airway diseases and highlight the influence of aging on airways' inflammation mechanism. The main goal of this review is to encourage research collaborations between experimentalist and modelers to promote our understanding of the physiological and pathological mechanisms that control inflammation in different airway diseases.
肺部炎症是机体对损伤的自然反应。它的作用是清除有害刺激物，如病原体、刺激物和受损细胞，并启动愈合过程。急性和慢性肺部炎症见于不同的呼吸系统疾病，如急性呼吸窘迫综合征、慢性阻塞性肺疾病（COPD）、哮喘和囊性纤维化（CF）。
在这篇综述中，我们发现 COPD 中的炎症反应是由呼吸道上皮细胞和巨噬细胞的激活决定的。上皮细胞和巨噬细胞释放转化生长因子-β（TGF-β），触发成纤维细胞增殖和组织重塑。哮喘导致气道高反应性、阻塞、黏液过度产生和气道壁重塑。细胞因子、过敏原、趋化因子和感染因子是激活哮喘上皮细胞信号通路的主要刺激物。CF 跨膜电导调节因子（CFTR）基因突变导致 CF。CFTR 的突变影响肺上皮固有免疫功能，导致过度和无效的气道炎症，无法消除肺部病原体。我们提出了基于常微分方程、偏微分方程和基于主体的模型的机制计算模型，这些模型已被应用于研究不同气道疾病中慢性炎症的复杂生理和病理机制。
本综述的范围是探讨气道疾病中的炎症机制，并强调衰老对气道炎症机制的影响。本综述的主要目的是鼓励实验家和建模者之间的研究合作，以促进我们对控制不同气道疾病中炎症的生理和病理机制的理解。
