气道基细胞,巨细胞和2型免疫之间的相互作用有助于在过敏性鼻炎中表皮屏障功能障碍
Emma Ruysseveldt1, Tine Wils1, Daan Rodiers1
1KU Leuven, Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Group, Leuven, Belgium.
过敏性鼻炎 (AR) 的基底细胞充当环境传感器,释放炎症信号. 然而,关键的过敏媒介会损害基底细胞功能,导致AR的呼吸道功能障碍.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 基底细胞功能障碍与慢性炎症性呼吸道疾病有关,特别是过敏性鼻炎 (AR),观察到上皮屏障缺陷,增生和转化等.
- 基础细胞前体功能的调节及其对AR2型炎症的特定贡献仍然不完全理解.
研究的目的:
- 调查过敏性鼻炎 (AR) 中鼻细胞的炎症和感觉作用.
- 阐明环境过敏原和炎症介质影响基底细胞功能的机制,并为AR病理生理学作出贡献.
主要方法:
- 来自健康个体和AR患者的初级鼻基细胞被用于体外研究.
- 检查了鼻子活检,以评估质细胞的存在和上皮相互作用.
- 功能测试评估了细胞因子/化学因子表达,细胞增殖,移动性,屏障形成和分化.
主要成果:
- Der p1过敏原诱导IL-6,CXCL1,CXCL6,CXCL8和SCF通过PAR2从基底细胞释放,突出显示它们的感觉和调节作用.
- 基底细胞衍生的SCF吸引了巨细胞进入上皮,这反过来又通过组胺素和酶诱导基底细胞进一步释放化学激素.
- 组胺,IL-4和IL-13损害了基底细胞的增殖,移动性,屏障功能和分化,这表明AR中的基底细胞功能障碍显著.
结论:
- 鼻基底细胞在AR中充当环境传感器和炎症调节器,释放关键细胞因子和化学因子.
- 基底细胞衍生干细胞因子 (SCF) 有助于巨细胞的招募,放大了AR的炎症级联.
- 过敏性炎症调解剂如组胺,IL-4和IL-13直接损害基底细胞功能,导致上皮功能障碍和AR中的疾病持续性.
更多相关视频
11:54Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
Published on: January 21, 2018
10:39Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
Published on: April 16, 2019
相关概念视频
Asthma-II: Pathophysiology and Classification
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Asthma: Pathogenesis and Management
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
Allergic Reactions
Allergic Drug Reactions
Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
