Worse than the Insult: The Role of Macrophages and Lymphocytes in Organic Dust-Induced Chronic Bronchitis

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Abstract
In livestock production settings, repetitive exposure to organic dust (OD) is a risk factor for chronic bronchitis (CB). Macrophages and lymphocytes cooperate to defend the lungs against inhaled dust, but when chronically activated, their actions contribute to chronic inflammation, oxidative stress, and tissue remodeling. Despite the strong body of literature examining the effects of OD exposure on leukocytes and lungs, the contribution of macrophages and lymphocytes to organic dust-associated chronic bronchitis is not fully understood. This review examines the role of macrophages and lymphocytes in organic dust-associated chronic bronchitis. To identify the body of literature addressing this goal, we conducted Boolean searches with keywords (e.g., bronchitis, leukocytes, organic dust) across four major databases: PubMed, Science Direct, Scopus, and Web of Science. From a total of 25,488 hits from all time, 18 research articles (from 2015 to 2025) provided contextual connection for explaining organic dust-associated chronic bronchitis. The results showed continuous or repetitive exposure to OD or its components (e.g., lipopolysaccharide) causes prolonged activation of macrophages and lymphocytes, which leads to overexpression of pro- and anti-inflammatory cytokines and chemokines via Toll-like receptor (TLR)4, TLR2, nuclear factor kappa B, protein kinase C, Extracellular Signal-Regulated Kinase (ERK), and Mitogen-Activated Protein Kinase (MAPK) pathways. Unresolved lung inflammation drives pathologic changes including mucus hypersecretion, airway remodeling, and onset of chronic bronchitis symptoms. Addition of micronutrients or other anti-inflammatory treatment helps to mitigate OD-induced lung inflammation. Defining the cellular and molecular contributions to organic dust-associated chronic bronchitis is essential for the development of targeted therapies that prevent or relieve prolonged airway inflammation.
Funding Information
  • National Institutes of Health (SC1HL150742)

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