Bacterial Biofilms and Increased Bacterial Counts Are Associated with Airway Stenosis

Abstract

Objectives:

The majority of airway stenoses are acquired secondary to the use of prolonged endotracheal intubation (ETT). Pressure exerted on the tracheal mucosa by the presence of ETT leads to irritation, ulceration, and granulation tissue formation and eventual fibrosis. An excess of granulation tissue promotes excess wound contracture. 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 was done to evaluate the difference between stenotic segment and normal trachea in terms of 1) presence of bacterial biofilms; 2) quantitative analysis of bacterial count; 3) inflammatory markers within tracheal tissue.

Methods:

Institutional review board approved case-control study, where cases were patients with airway stenosis and controls were patients without airway stenosis. We performed scanning electron microscopy (SEM) for biofilm, quantitative polymerase chain reaction (qPCR) for quantitative analysis of bacterial count, and immunohistochemistry (IHC) for inflammatory markers.

Results:

SEM showed presence of biofilm in cases compared to controls. The number of 16S rRNA gene copies using qPCR, a surrogate for the number of bacterial cells, was significantly higher in cases (mean=198) compared to controls (mean=30 ) (P < 0.05). Pediatric cases showed a significantly higher bacterial count than adult cases. IHC showed stronger staining for SMAD3 and transforming growth factor β (TGF-β).

Conclusions:

Biofilms are present in airway stenotic segments, and there exists a difference in tracheal microbiomes and inflammatory markers between patients with airway stenosis and normal controls.