Linked Life Data

16893395

Source:http://linkedlifedata.com/resource/pubmed/id/16893395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-8-8
pubmed:abstractText
Aspergillus fumigatus is ubiquitous and yet causes invasive, chronic and allergic disease of the lung. Chronic cavitary pulmonary aspergillosis (CCPA) is a slowly destructive form of pulmonary aspergillosis, without immunocompromise. We hypothesized that CCPA cytokine gene polymorphisms would differ from patients with allergic bronchopulmonary aspergillosis (ABPA) and uninfected controls. We have profiled functional cytokine gene polymorphisms for interleukin (IL)-10, IL-15, transforming growth factors (TGF)-beta1, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma in patients with CCPA (n = 24) who were compared with other forms of aspergillosis (mostly ABPA) (n = 15) and with ethnically matched controls (n = 65-330). Results are described with reference to the high-producing genotype in each case. Susceptibility to aspergillosis (all patients compared with normal controls) was associated with higher frequency of the IL-15 +13689*A allele (OR = 2.37, P = 0.0028) and A/A genotype (chi(2) = 10.31, P < 0.001), with a lower frequency of the TNF-alpha-308*A/A genotype (chi(2) = 11.05, P < 0.01). Within the aspergillosis patients, CCPA is associated with lower frequency of the IL-10 -1082*G allele (OR = 0.38, P = 0.0006) and G/G genotype (chi(2) = 22.45, P < 0.001) and with a lower frequency of the TGF-beta1 +869 *T allele (OR +0.42, P < 0.0029) and T/T genotype (chi(2) = 17.82, P < 0.001) compared with non-CCPA patients and normal controls. Patients infected with Aspergillus appear to be higher producers of IL-15, a Th2-promoting cytokine, and lower producers of TNF-alpha, a cytokine central in protective responses. CCPA occurs in patients who are genetically lower producers of both IL-10 and TGF-beta1. As these cytokines are regulatory and anti-inflammatory, CCPA may be a consequence of poor inflammatory response control in the lung.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1744-3121
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
297-302
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16893395-Adult, pubmed-meshheading:16893395-Aspergillosis, pubmed-meshheading:16893395-Aspergillosis, Allergic Bronchopulmonary, pubmed-meshheading:16893395-Aspergillus fumigatus, pubmed-meshheading:16893395-Case-Control Studies, pubmed-meshheading:16893395-Cytokines, pubmed-meshheading:16893395-England, pubmed-meshheading:16893395-Genetic Predisposition to Disease, pubmed-meshheading:16893395-Genotype, pubmed-meshheading:16893395-Humans, pubmed-meshheading:16893395-Interferon-gamma, pubmed-meshheading:16893395-Interleukin-10, pubmed-meshheading:16893395-Interleukin-15, pubmed-meshheading:16893395-Lung Diseases, Fungal, pubmed-meshheading:16893395-Middle Aged, pubmed-meshheading:16893395-Polymerase Chain Reaction, pubmed-meshheading:16893395-Sinusitis, pubmed-meshheading:16893395-Transforming Growth Factor beta, pubmed-meshheading:16893395-Transforming Growth Factor beta1, pubmed-meshheading:16893395-Tumor Necrosis Factor-alpha
pubmed:year
2006
pubmed:articleTitle
Cytokine profiling of pulmonary aspergillosis.
pubmed:affiliation
The School of Medicine, The University of Manchester, Oxford Road, Manchester, UK.
pubmed:publicationType
Journal Article