Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-5-30
pubmed:abstractText
Mast cells and basophils contribute to induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes. The latter include a variety of stimuli that have only recently been elucidated, including mechanisms triggered by bacteria, virus, fungi, complement, or autoantibodies. MCs, and basophils contribute to inflammation both directly through the release of inflammatory mediators, cytokines and growth factors and indirectly through the activation of structural cells. Accumulating evidence places MCs (and most probably basophils) in a position of importance in the pathogenesis of CRS, particularly in the pathogenesis and progression of NP (Fig. 1). Mechanisms other than conventional IgE-dependent activation of MCs are intriguing as potential mechanisms of eosinophilic inflammation in non-allergic CRS/NP. Although it is not possible using current pharmacologic approaches to completely isolate the effects of MCs or basophils in CRS and NP pathogenesis, it seems most likely that such approaches will eventually be available. It might be expected that one or both of these cells will be shown to play important roles, particularly considering their potential for activation by IgE and non-IgE mechanisms, their production of a broad array of inflammatory mediators, cytokines and growth factors, and their unique assortment of proteases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1075-7910
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
93-101
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Role of mast cells and basophils in chronic rhinosinusitis.
pubmed:affiliation
Department of Otolaryngology, Nippon Medical School, Tokyo, Japan.
pubmed:publicationType
Journal Article, Review