Chavda Vivek P, Bezbaruah Rajashri, Ahmed Nasima, Alom Shahnaz, Bhattacharjee Bedanta, Nalla Lakshmi Vineela, Rynjah Damanbhalang, Gadanec Laura Kate, Apostolopoulos Vasso
Department of Pharmaceutics and Pharmaceutical Technology, L.M. College of Pharmacy, Ahmedabad 380009, Gujarat, India.
Department of Pharmaceutical Sciences, Faculty of Science and Engineering, Dibrugarh University, Dibrugarh 786004, Assam, India.
Cells. 2025 Mar 9;14(6):400. doi: 10.3390/cells14060400.
Pulmonary homeostasis can be agitated either by external environmental insults or endogenous factors produced during respiratory/pulmonary diseases. The lungs counter these insults by initiating mechanisms of inflammation as a localized, non-specific first-line defense response. Cytokines are small signaling glycoprotein molecules that control the immune response. They are formed by numerous categories of cell types and induce the movement, growth, differentiation, and death of cells. During respiratory diseases, multiple proinflammatory cytokines play a crucial role in orchestrating chronic inflammation and structural changes in the respiratory tract by recruiting inflammatory cells and maintaining the release of growth factors to maintain inflammation. The issue aggravates when the inflammatory response is exaggerated and/or cytokine production becomes dysregulated. In such instances, unresolving and chronic inflammatory reactions and cytokine production accelerate airway remodeling and maladaptive outcomes. Pro-inflammatory cytokines generate these deleterious consequences through interactions with receptors, which in turn initiate a signal in the cell, triggering a response. The cytokine profile and inflammatory cascade seen in different pulmonary diseases vary and have become fundamental targets for advancement in new therapeutic strategies for lung diseases. There are considerable therapeutic approaches that target cytokine-mediated inflammation in pulmonary diseases; however, blocking specific cytokines may not contribute to clinical benefit. Alternatively, broad-spectrum anti-inflammatory approaches are more likely to be clinically effective. Herein, this comprehensive review of the literature identifies various cytokines (e.g., interleukins, chemokines, and growth factors) involved in pulmonary inflammation and the pathogenesis of respiratory diseases (e.g., asthma, chronic obstructive pulmonary, lung cancer, pneumonia, and pulmonary fibrosis) and investigates targeted therapeutic treatment approaches.
肺部稳态可因外部环境损伤或呼吸/肺部疾病期间产生的内源性因素而受到干扰。肺部通过启动炎症机制作为局部、非特异性的一线防御反应来对抗这些损伤。细胞因子是控制免疫反应的小信号糖蛋白分子。它们由多种细胞类型形成，并诱导细胞的移动、生长、分化和死亡。在呼吸系统疾病期间，多种促炎细胞因子通过募集炎症细胞和维持生长因子的释放以维持炎症，在协调慢性炎症和呼吸道结构变化中起关键作用。当炎症反应过度和/或细胞因子产生失调时，问题会加剧。在这种情况下，无法解决的慢性炎症反应和细胞因子产生会加速气道重塑和不良适应性后果。促炎细胞因子通过与受体相互作用产生这些有害后果，进而在细胞中启动信号，触发反应。不同肺部疾病中所见的细胞因子谱和炎症级联反应各不相同，已成为肺部疾病新治疗策略进展的基本靶点。有相当多针对肺部疾病中细胞因子介导炎症的治疗方法；然而，阻断特定细胞因子可能不会带来临床益处。相比之下，广谱抗炎方法更可能具有临床疗效。在此，本全面的文献综述确定了参与肺部炎症和呼吸系统疾病（如哮喘、慢性阻塞性肺病、肺癌、肺炎和肺纤维化）发病机制的各种细胞因子（如白细胞介素、趋化因子和生长因子），并研究了靶向治疗方法。
