The bronchial epithelium in chronic and severe asthma

被引:21
作者
Davies D.E. [1 ]
机构
[1] Respiratory, Cell & Molecular Biology Division, School of Medicine, University of Southampton, Level D Centre Block, Southampton General Hospital, Tremona Rd, Southampton
关键词
Allergy Clin Immunol; Asthma; Bronchial Epithelial Cell; Respir Crit; Severe Asthma;
D O I
10.1007/s11882-001-0080-9
中图分类号
学科分类号
摘要
Although patients with severe, steroid-refractory asthma represent a minor proportion of the asthmatic population, they consume a disproportionate amount of healthcare costs and have a greatly impaired quality of life. They respond poorly to conventional anti-inflammatory therapy and frequently exhibit a component of fixed airflow obstruction that has been linked to airway wall remodeling. In addition to its classic barrier function, the bronchial epithelium responds to changes in the external environment by secreting cytoprotective molecules and mediators that signal to cells of the immune system. In asthma, the bronchial epithelium is stressed and damaged, with shedding of the columnar cells into the airway lumen. This damage and ensuing repair responses are proposed to orchestrate airway inflammation and remodeling via activation of myofibroblasts in the underlying lamina reticularis. This allows the two cell types to work as a trophic unit, propagating and amplifying the response at the cell surface into the submucosa. Because wound healing involves inflammation, repair, and remodeling processes, this review considers the evidence that exaggerated inflammation and remodeling of the airways arise as a consequence of abnormal injury and repair responses coordinated by the bronchial epithelium, highlighting, where possible, steroid-insensitive components. © 2001, Current Science Inc.
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页码:127 / 133
页数:6
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共 58 条
  • [11] Busse W.W., Elias J., Sheppard D., Banks-Schlegel S., Airway remodelling and repair, Am J Respir Crit Care Med, 160, pp. 1035-1042, (1999)
  • [12] Chung K.F., Godard P., Adelroth E., Et al., Difficult therapy resistant asthma: an ERS Task Force Report, Eur Respir Rev, 10, pp. 1-101, (2000)
  • [13] Pearce N., Pekkanen J., Beasley R., How much asthma is really attributable to atopy?, Thorax, 54, pp. 268-272, (1999)
  • [14] Lau S., Illi S., Sommerfeld C., Et al., Early exposure to housedust mite and cat allergens and development of childhood asthma: a cohort study: Multicentre Allergy Study Group, Lancet, 356, pp. 1392-1397, (2000)
  • [15] Jansen D.F., Rijcken B., Schouten J.P., Et al., The relationship of skin test positivity, high serum total IgE levels, and peripheral blood eosinophilia to symptomatic and asymptomatic airway hyperresponsiveness, Am J Respir Crit Care Med, 159, pp. 924-931, (1999)
  • [16] Holgate S.T., Genetic and environmental interaction in allergy and asthma, J Allergy Clin Immunol, 104, pp. 1139-1146, (1999)
  • [17] Stein R.T., Holberg C.J., Sherrill D., Et al., Influence of parental smoking on respiratory symptoms during the first decade of life: the Tucson Children’s Respiratory Study, Am J Epidemiol, 149, pp. 1030-1037, (1999)
  • [18] Nicolai T., Environmental air pollution and lung disease in children, Monaldi Arch Chest Dis, 54, pp. 475-478, (1999)
  • [19] Johnston S.L., Pattemore P.K., Sanderson G., Et al., The relationship between upper respiratory infections and hospital admissions for asthma: a time-trend analysis, Am J Respir Crit Care Med, 154, pp. 654-660, (1996)
  • [20] Holgate S.T., Clinical characteristics associated to severe asthma, Am J Respir Crit Care Med, 159, (1999)