Abstract
Inhalation of organic dusts in agricultural environments causes airway inflammatory diseases. Despite advances in understanding the airway response to dust-induced inflammation, less is known about the transition from lung injury to repair and recovery. The objective of this study was to define the post-inflammation homeostasis events following organic dust-induced lung injury. Using an established protocol, mice were intranasally treated with swine confinement facility organic dust extract (ODE) daily for 3 weeks (repetitive exposure) or treated daily with ODE for 3 weeks followed by no treatment for 1–4 weeks (recovery period) whereupon lavage fluid, lung tissue, and sera were processed. During recovery period, a significant decrease was observed in ODE-induced neutrophil levels after 1 week, lymphocytes at 2 weeks, and macrophages at 4 weeks in the lavage fluid. ODE-induced lung cellular aggregates and bronchiolar compartment inflammation were diminished, but persisted for 4 weeks post-injury. Alveolar inflammation resolved at 3 weeks. ODE-induced lung neutrophils were cleared by 3 weeks, B-cells by 2 weeks, and CD3+CD4+ and CD3+CD8+ T cells by 4 week recovery period. Collectively, these results identify important processes during recovery period following agricultural dust-induced inflammation, and present possible strategies for improving lung repair and resolution.
Highlights
Inhalation of agricultural organic dusts cause injury and inflammation in the lungs of exposed workers [1,2]
It has been established that repetitive organic dust extract (ODE) treatment induces the influx of neutrophils, macrophages, and lymphocytes, and that airway macrophages and lymphocytes remain increased at one week following final ODE treatment [12]
We investigated the temporal course for the resolution of repetitive ODE-induced inflammatory cell influx (Figure 1)
Summary
Inhalation of agricultural organic dusts cause injury and inflammation in the lungs of exposed workers [1,2]. The composition of agricultural dust is complex, but is known to contain gram positive and gram negative microbial cell wall components, proteases, and particulate matter [3,7,8]. This complex organic dust activates several lung innate immune pathways that otherwise may not be activated in single agent (e.g., endotoxin, bleomycin) exposure injury models [6,9]. TLR2 and TLR4 gene polymorphisms have been implicated in modulating lung disease in swine workers [14,15]
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