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.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0743-x) contains supplementary material, which is available to authorized users.

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Background: Particulate matter (PM) air pollution causes deleterious health effects; however, less is known about health effects of indoor air particulate matter (IAP). Objective: To understand whether IAP influences distinct mechanisms in the development of respiratory tract infections, including bacterial growth, biofilm formation, and innate immunity. Additionally, we tested whether IAP from Iowa houses of subjects with and without recent respiratory exacerbations recapitulated the National Institute of Standards and Technology (NIST) IAP findings. Methods: To test the effect of NIST and Iowa IAP on bacterial growth and biofilm formation, we assessed Staphylococcus aureus growth and Pseudomonas aeruginosa biofilm formation with and without the presence of IAP. To assess the effect of IAP on innate immunity, we exposed primary human airway surface liquid (ASL) to NIST, and Iowa IAP. Lastly, we tested whether specific metals may be responsible for effects on airway innate immunity. Results: NIST and Iowa IAP significantly enhanced bacterial growth and biofilm formation. NIST IAP (whole particle and the soluble portion) impaired ASL antimicrobial activity. IAP from one Iowa home significantly impaired ASL antimicrobial activity (p < 0.05), and five other homes demonstrated a trend (p ≤ 0.18) of impaired ASL antimicrobial activity. IAP from homes of subjects with a recent history of respiratory exacerbation tended (p = 0.09) to impair ASL antimicrobial activity more than IAP from homes of those without a history respiratory exacerbation. Aluminum and Magnesium impaired ASL antimicrobial activity, while copper was bactericidal. Combining metals varied their effect on ASL antimicrobial activity. Stapleton et al. Indoor PM Affects Respiratory Health Conclusions: NIST IAP and Iowa IAP enhanced bacterial growth and biofilm formation. ASL antimicrobial activity was impaired by NIST IAP, and Iowa house IAP from subjects with recent respiratory exacerbation tended to impair ASL antimicrobial activity. Individual metals may explain impaired ASL antimicrobial activity; however, antimicrobial activity in the presence of multiple metals warrants further study.

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