Abstract
BackgroundSmoking is a leading cause of respiratory infections worldwide. Tobacco particulate matter disrupts iron homeostasis in the lungs and increases the iron content in the airways of smokers. The airway epithelia secrete lactoferrin to quench iron required for bacteria to proliferate and cause lung infections. We hypothesized that smokers would have increased bacterial growth and biofilm formation via iron lactoferrin imbalance.MethodsWe collected bronchoalveolar lavage (BAL) samples from non-smokers and smokers. We challenged these samples using a standard inoculum of Staphylococcus aureus and Pseudomonas aeruginosa and quantified bacterial growth and biofilm formation. We measured both iron and lactoferrin in the samples. We investigated the effect of supplementing non-smoker BAL with cigarette smoke extract (CSE) or ferric chloride and the effect of supplementing smoker BAL with lactoferrin on bacterial growth and biofilm formation.ResultsBAL from smokers had increased bacterial growth and biofilm formation compared to non-smokers after both S. aureus and P. aeruginosa challenge. In addition, we found that samples from smokers had a higher iron to lactoferrin ratio. Supplementing the BAL of non-smokers with cigarette smoke extract and ferric chloride increased bacterial growth. Conversely, supplementing the BAL of smokers with lactoferrin had a concentration-dependent decrease in bacterial growth and biofilm formation.ConclusionCigarette smoking produces factors which increase bacterial growth and biofilm formation in the BAL. We propose that smoking disrupts the iron-to-lactoferrin in the airways. This finding offers a new avenue for potential therapeutic interventions to prevent respiratory infections in smokers.
Highlights
Smoking is a leading cause of respiratory infections worldwide
Bacteria grows more in the bronchoalveolar lavage (BAL) from smokers compared to non-smokers We hypothesized that BAL from smokers would have increase bacterial growth compared to non-smokers
Bacteria develops more biofilm mass in the BAL from smokers compared to non-smokers Since BAL from smokers had more S. aureus and P. aeruginosa growth compared to non-smokers, we investigated the ability of these bacteria to form biofilms
Summary
Smoking is a leading cause of respiratory infections worldwide. Tobacco particulate matter disrupts iron homeostasis in the lungs and increases the iron content in the airways of smokers. The airway epithelia secrete lactoferrin to quench iron required for bacteria to proliferate and cause lung infections. We hypothesized that smokers would have increased bacterial growth and biofilm formation via iron lactoferrin imbalance. Respiratory infections are one of the leading causes of mortality worldwide and smoking is considered a risk factor for developing upper and lower respiratory infections [1,2,3]. Exposure to cigarette smoke is associated with increased risk of airway bacterial colonization compared to non-smokers [4, 5]. One of the most abundant AMPs present in the ASL is lactoferrin, a bacteriostatic protein that chelates iron, which is required for bacteria to grow and form biofilms [13]. The impairment of AMP activity plays a fundamental role in the origin of infectious lung diseases. Several factors can alter the activity of AMPs such as decreased pH, increased
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