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BMC pulmonary medicine, 2017-11, Vol.17 (1), p.159-159, Article 159
2017
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Autor(en) / Beteiligte
Titel
Tobacco-smoking induced GPR15-expressing T cells in blood do not indicate pulmonary damage
Ist Teil von
  • BMC pulmonary medicine, 2017-11, Vol.17 (1), p.159-159, Article 159
Ort / Verlag
England: BioMed Central Ltd
Erscheinungsjahr
2017
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
  • Recently, it was shown that chronic tobacco smoking evokes specific cellular and molecular changes in white blood cells by an excess of G protein-coupled receptor 15 (GPR15)-expressing T cells as well as a hypomethylation at DNA CpG site cg05575921 in granulocytes. In the present study, we aimed to clarify the general usefulness of these two biomarkers as putative signs of non-cancerous change in homeostasis of the lungs. In a clinical cohort consisting of 42 patients with chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD) and pneumonia and a control cohort of 123 volunteers, the content of GPR15-expressing blood cells as well as the degree of methylation at cg05575921 were analysed by flow-cytometry and pyrosequencing, respectively. Smoking behaviour was estimated by questionnaire and cotinine level in plasma. Never-smoking patients could be distinguished from former and current smokers by both the proportion of GPR15-expressing T cells as well as cg05575921 methylation in granulocytes, with 100% and 97% specificity and 100% sensitivity, respectively. However, both parameters were not affected by lung diseases. The degrees of both parameters were not changed neither in non-smoking nor smoking patients, compared to appropriate control cohorts of volunteers. The degree of GPR15-expressing cells among T cells as well as the methylation at cg05575921 in granulocytes in blood are both rather signs of tobacco-smoking induced systemic inflammation because they don't indicate specifically non-cancerous pathological changes in the lungs.
Sprache
Englisch
Identifikatoren
ISSN: 1471-2466
eISSN: 1471-2466
DOI: 10.1186/s12890-017-0509-0
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_455ca96df0eb4490b37e126c56832870

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