Cells and Cytokines in Chronic Bronchial Infection

Up-regulation of circulating adhesionmolecules in bronchiectasis

“…Intensive neutrophil recruitment into the airways and their subsequent migration into the airway lumen, clinically manifested as sputum production, are hallmarks in the pathogenesis of bronchiectasis [1,2]. This is associated with a prolific production in pro-inflammatory mediators, such as IL-1, IL-8, TNF-a, and leukotriene B 4 (LTB 4 ) in the bronchiectatic airways [1,21].…”

“…This is associated with a prolific production in pro-inflammatory mediators, such as IL-1, IL-8, TNF-a, and leukotriene B 4 (LTB 4 ) in the bronchiectatic airways [1,21]. While the role of these pro-inflammatory mediators in the recruitment of neutrophils into the tracheobronchial tree has recently been established [1, 22, 25±27], little is known about the interaction between neutrophils and endothelial cells in the pathogenesis of bronchiectasis.…”

“…There is also a mononuclear cell infiltration, including CD4+ T cells and CD68+ macrophages, into the bronchiectatic airways, although the role of these cells in the pathogenesis is unclear [35]. The up-regulation of circulating VCAM-1 among bronchiectasis patients could be secondary to stimuli on the airway endothelium by bacterial derived LPS, or local inflammatory cytokine such as TNF-a and IL-1 production [1]. It is also possible that in vivo VCAM-1 up-regulation serves to recruit nonneutrophil leukocytes, namely monocytes and lymphocytes, into the bronchiectasis airways, while ICAM-1 and E-selectin recruit the neutrophils [19, 20, 29±34].…”

“…Intense neutrophil influx into the airways occurs in bronchiectasis [1,2] which could be harmful when neutrophil products, particularly elastase, are released in response to bacterial infection [3±6].There is increasing evidence to suggest that the recruitment of neutrophils contributes to continued airway damage in bronchiectasis [3±6]. Adhesion molecules, expressed on the surface of endothelial cells and leukocytes [7±9], mediate migration of leukocytes from the vascular compartment into inflamed tissue.…”

“…Unlike ICAM:-1, endothelial cells [19,20] do not normally express VCAM-1. The expression of these adhesion molecules are up-regulated following exposure to pro-inflammatory cytokines including interleukin-1 (IL-1), tumour necrosis factor-a (TNF-a), and bacterial lipopolysaccharide (LPS) [11±13, 18±20], which are abundant in the airways of patients with bronchiectasis [1,21]. The soluble isoforms of these adhesion molecules can be found in the circulation, and have been increasingly recognized as markers of inflammation and endothelial activation [22].…”