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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nasal polyps are common, affecting one to four per cent of the population. Their cause, however, remains unknown and it is possible that it is not the same in all patients. They have a clear association with asthma, aspirin sensitivity and cystic fibrosis. Histologically they demonstrate large quantities of extracellular fluid, mast cell degranulation and an infiltrate of inflammatory cells, usually eosinophils. While this appearance would suggest an allergic pathology there is little conclusive evidence to support this in most patients. There is, however, some preliminary evidence to suggest that a local allergic process could be the cause. While allergic fungal sinusitis is a well defined clinical entity with recognized diagnostic criteria the ubiquitous nature of fungal spores makes the role of fungal infection in patients with nasal polyps difficult to determine and currently this remains unclear. Surgical treatment of nasal polyps has declined in recent years as the benefits of medical treatment have become increasingly recognized. There is good evidence to support the use of corticosteroids both as a primary and post-operative treatment in the majority of patients. Other medical treatments require further evaluation before they could be considered a viable alternative to steroids. Assessment of the literature regarding surgical intervention is difficult and there is little evidence on which to base a surgical treatment philosophy. The authors believe that an endoscopic approach using a microdebrider facilitates accurate removal of polyps with preservation of normal anatomy.
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PMID:Nasal polyps: still more questions than answers. 1259 Aug 49

Immunosuppressed patients are frequently afflicted with severe mycoses caused by opportunistic fungal pathogens. Besides being a commensal, colonizing predominantly skin and mucosal surfaces, Candida albicans is the most common human fungal pathogen. Mast cells are present in tissues prone to fungal colonization being expectedly among the first immune cells to get into contact with C. albicans. However, mast cell-fungus interaction remains a neglected area of study. Here we show that human mast cells mounted specific responses towards C. albicans. Collectively, mast cell responses included the launch of initial, intermediate and late phase components determined by the secretion of granular proteins and cytokines. Initially mast cells reduced fungal viability and occasionally internalized yeasts. C. albicans could evade ingestion by intracellular growth leading to cellular death. Furthermore, secreted factors in the supernatants of infected cells recruited neutrophils, but not monocytes. Late stages were marked by the release of cytokines that are known to be anti-inflammatory suggesting a modulation of initial responses. C. albicans-infected mast cells formed extracellular DNA traps, which ensnared but did not kill the fungus. Our results suggest that mast cells serve as tissue sentinels modulating antifungal immune responses during C. albicans infection. Consequently, these findings open new doors for understanding fungal pathogenicity.
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PMID:Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells. 2619 81