ArticleAmerican journal of respiratory cell and molecular biology2012
CD11c(+)/CD11b(+) cells are critical for organic dust-elicited murine lung inflammation.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
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- Lung-delivered IL-10 mitigates Lung inflammation induced by repeated endotoxin exposures in male mice.Physiological reports · 2025Article
- Aconitate decarboxylase 1 mediates the acute airway inflammatory response to environmental exposures.Frontiers in immunology · 2024Article
- Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure.Journal of immunotoxicology · 2023Article
- Agricultural dust derived bacterial extracellular vesicle mediated inflammation is attenuated by DHA.Scientific reports · 2023Article
- Neutralization of IL-33 modifies the type 2 and type 3 inflammatory signature of viral induced asthma exacerbation.Respiratory research · 2021Article
- Lung Inflammatory Response to Environmental Dust Exposure in Mice Suggests a Link to Regional Respiratory Disease Risk.Journal of inflammation research · 2021Article
- Article
- Organic dust-induced lung injury and repair: Bi-directional regulation by TNFα and IL-10.Journal of immunotoxicology · 2020Article
- A High Docosahexaenoic Acid Diet Alters the Lung Inflammatory Response to Acute Dust Exposure.Nutrients · 2020Article
- Molecular and cellular mechanisms linking air pollution and bone damage.Environmental research · 2020Review
- MyD88 regulates a prolonged adaptation response to environmental dust exposure-induced lung disease.Respiratory research · 2020Article
- Amphiregulin modulates murine lung recovery and fibroblast function following exposure to agriculture organic dust.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Association Between Organic Dust Exposure and Adult-Asthma: A Systematic Review and Meta-Analysis of Case-Control Studies.Allergy, asthma & immunology research · 2019Article
- Identification of an Increased Alveolar Macrophage Subpopulation in Old Mice That Displays Unique Inflammatory Characteristics and Is Permissive toJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- Combined Collagen-Induced Arthritis and Organic Dust-Induced Airway Inflammation to Model Inflammatory Lung Disease in Rheumatoid Arthritis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Organic dust, causing both oxidative stress and Nrf2 activation, is phagocytized by bronchial epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Relationship of systemic IL-10 levels with proinflammatory cytokine responsiveness and lung function in agriculture workers.Respiratory research · 2018Article
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Organic dust exposure in the agricultural industry results in significant lung disease. Macrophage infiltrates are increased in the lungs after organic dust exposures, yet the phenotype and functional importance of these cells remain unclear. Using an established intranasal inhalation murine model of dust-induced lung inflammation, animals were treated once or daily for 3 weeks with swine confinement organic dust extract (DE). Repetitive DE treatment for 3 weeks resulted in significant increases in CD11c(+)/CD11b(+) macrophages in whole lung-associated tissue. These cells displayed increased costimulatory molecule (CD80 and CD86) expression, enhanced phagocytic ability, and an increased production of IL-6, CXCL1, and CXCL2. Similar findings were observed with the CD11c(+)/CD11b(+) macrophage infiltrate after repetitive exposure to peptidoglycan, a major DE component. To determine the functional importance of macrophages in mediating DE-induced airway inflammation, lung macrophages were selectively depleted using a well-established intranasal clodronate liposome depletion/suicide strategy. First, macrophage depletion by clodronate liposomes resulted in significant reductions in airway neutrophil influx and TNF-α and IL-6 production after a single exposure to DE. In contrast, after repetitive 3-week exposure to DE, airway lavage fluid and lung tissue neutrophils were significantly increased in clodronate liposome-treated mice compared with control mice. A histological examination of lung tissue demonstrated striking increases in alveolar and bronchiolar inflammation, as well as in the size and distribution of cellular aggregates in clodronate-liposome versus saline-liposome groups repetitively exposed to DE. These studies demonstrate that DE elicits activated CD11c(+)/CD11b(+) macrophages in the lung, which play a critical role in regulating the outcome of DE-induced airway inflammation.
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Registered trials
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