Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the mechanisms involved in the action of new macrolides on chronic sinusitis, we examined the effects of clarithromycin (CAM) and roxiythromycin (RXM) on the expression of adhesion molecules (L-selectin and Mac-1) on peripheral blood neutrophils of individuals with chronic sinusitis. The administration of CAM and RXM slightly inhibited the down-regulation of L-selectin expression on neutrophils induced by interleukin (IL)-8 stimulation. Furthermore, the administration of CAM strongly inhibited the IL-8-induced up-regulation of Mac-1 expression on neutrophils. These observations suggest that the new macrolides such as CAM and RXM may affect the functions of neutrophils in chronic sinusitis by modulating the expression of L-selectin and Mac-1 molecules on neutrophils, thereby attenuating the adhesion of neutrophils.
Auris Nasus Larynx 2002 Jul
PMID:Effect of new macrolides on the expression of adhesion molecules on neutrophils in chronic sinusitis. 1216 49

Bronchial asthma is a chronic disorder characterized by airway inflammation, reversible airway obstruction, and airway hyperresponsiveness. Eosinophils are believed to play important roles in the pathogenesis of asthma through the release of inflammatory mediators. In refractory eosinophilic asthma, anti-IL-5 mAb reduces exacerbations and steroid dose, indicating roles of eosinophils and IL-5 in the development of severe eosinophilic asthma. Even in the absence of IL-5, it is likely that the "Th2 network", including a cascade of vascular cell adhesion molecule-1/CC chemokines/GM-CSF, can sufficiently maintain eosinophilic infiltration and degranulation. Cysteinyl leukotrienes can also directly provoke eosinophilic infiltration and activation in the airways of asthma. Therefore, various mechanisms would be involved in the eosinophilic airway inflammation of asthma. In the pathogenesis of severe asthma, not only eosinophils but also mast cells or neutrophils play important roles. Mast cells are much infiltrated to smooth muscle in severe asthma and induce airway remodeling by release of inflammatory mediators such as amphiregulin. Treatment with anti-IgE Ab, which neutralizes circulating IgE and suppresses mast cell functions, reduces asthma exacerbations in severe asthmatic patients. Furthermore, infiltration of neutrophils in the airway is also increased in severe asthma. IL-8 plays an important role in the accumulation of neutrophils and is indeed upregulated in severe asthma. In the absence of chemoattractant for eosinophils, neutrophils stimulated by IL-8 augment the trans-basement membrane migration of eosinophils, suggesting that IL-8-stimulated neutrophils could lead eosinophils to accumulate in the airways of asthma. In view of these mechanisms, an effective strategy for controlling asthma, especially severe asthma, should be considered.
Auris Nasus Larynx 2011 Oct
PMID:Pathogenesis of airway inflammation in bronchial asthma. 2133 36