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• W2169391303 abstract "ObjectivesMost airway stenoses are acquired secondary to the use of prolonged endotracheal intubation. Antibiotics have been shown to decrease local inflammation and granulation tissue formation in the trachea. However, antibiotic therapy is not 100% effective in preventing or treating granulation tissue formation. Development of bacterial biofilms may explain this finding. This study evaluates the difference between tracheal stenotic segments and normal trachea in terms of (1) presence of bacterial biofilms, (2) quantitative bacterial counts, and (3) inflammatory markers. SubjectsA total of 12 patients were included in the study. Tissue from stenotic segments from 6 patients with airway stenosis undergoing open airway procedures were compared with tracheal tissue from 6 patients without airway stenosis undergoing tracheostomy. MethodsScanning electron microscopy for biofilm detection, quantitative polymerase chain reaction for quantitative analysis of bacterial count, and immunohistochemistry were performed for inflammatory markers transforming growth factor β1 (TGF-β1) and SMAD3. ResultsCompared with the patients without airway stenosis, patients in the airway stenosis group showed presence of bacterial biofilms, a significantly higher expression of 16S rRNA gene copies per microgram of tissue (187.5 vs 7.33, P = .01), and higher expression of TGF-β1 (91% vs 8%, P < .001) and SMAD3 (83.5% vs 17.8%, P < .001). ConclusionBacterial biofilms, increased bacterial counts, and higher expression of TGF-β1 and SMAD3 are associated with airway stenosis." @default.
• W2169391303 created "2016-06-24" @default.
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• W2169391303 date "2014-02-10" @default.
• W2169391303 modified "2023-09-27" @default.
• W2169391303 title "Bacterial Biofilms and Increased Bacterial Counts Are Associated with Airway Stenosis" @default.
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• W2169391303 doi "https://doi.org/10.1177/0194599814522765" @default.
• W2169391303 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24515969" @default.
• W2169391303 hasPublicationYear "2014" @default.
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