Subglottic stenosis (SGS) is a significant health care complication following intubation in pediatric intensive care units. In the United States, SGS impacts nearly 8% of over 20,000 early-term patients annually, leading to comorbidities such as congenital heart disease and central nervous system disorders. In SGS, fibroblasts deposit aberrant extracellular matrix resulting in a fibrous scar and airway narrowing between the vocal folds and the inferior border of the cricoid cartilage. Most cases require repeated endoscopic interventions to open the airway and severe cases require invasive surgeries like laryngotracheal reconstruction. Independent of severity, most SGS patients experience major complications such as restenosis and laryngeal edema and are left with severe dysphonia, dyspnea, and cognitive delays. Airway fibrosis is largely driven by inflammation with known dysregulation in pro-healing macrophages, CD4+, and γδ T cells, among others. Bacterial-host interactions are paramount in the airway for both maintaining homeostasis and driving pathogenesis, which has been observed in many diseases such as rhinosinusitis, asthma, as well as subglottic stenosis. Therefore, the goal of this work is to define the role of bacteria in SGS and engineer a preventative treatment by controlling the microbiome. Although conventional antibiotics and steroids are prescribed to reduce infection and inflammation, physicians advise against them as the risk of multi-drug resistance and growth retardation outweigh the potential benefits. Therefore, we use antimicrobial peptides (AMPs), small, naturally occurring biomolecules that physically disrupt microbial membranes thus avoiding the risk of multi-drug resistance and side effects of small molecule antibiotics as they protect the commensal, healthy microbiome and are biocompatible native tissues. In this study, to design a treatment that will prevent SGS, we compare the airway transcriptome and microbiome of patients with SGS and corroborate the findings in an established SGS mouse model. In parallel, we engineer a localized delivery platform by coating endotracheal tubes (ETs) to target AMP delivery and microbiome modulation. We hypothesize that dysregulated laryngotracheal bacterial communities accelerate SGS by inducing inflammatory cell infiltration and fibroblast differentiation, which is prevented by locally administering AMPs to modulate the microbiome by coated ETs.