ArticleShock (Augusta, Ga.)2014
Interleukin 10 overexpression alters survival in the setting of gram-negative pneumonia following lung contusion.
Article in Shock (Augusta, Ga.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
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- Dynamic monitoring of kidney injury status over 3 days in the intensive care unit as a sepsis phenotype associated with hospital mortality and hyperinflammation.Biomedical journal · 2022Article
- Out-Smarting the Host: Bacteria Maneuvering the Immune Response to Favor Their Survival.Frontiers in immunology · 2020Review
- Loss of myeloid-specific protein phosphatase 2A enhances lung injury and fibrosis and results in IL-10-dependent sensitization of epithelial cell apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Klebsiella pneumoniae infection biology: living to counteract host defences.FEMS microbiology reviews · 2019Review
- Correction to: A new multiple trauma model of the mouse.BMC musculoskeletal disorders · 2019Article
- Electroporation-mediated delivery of FER gene enhances innate immune response and improves survival in a murine model of pneumonia.Gene therapy · 2018Article
- A new multiple trauma model of the mouse.BMC musculoskeletal disorders · 2017Article
- Electroporation-mediated delivery of the FER gene in the resolution of trauma-related fatal pneumonia.Gene therapy · 2016Article
- Plasma Inflammatory Cytokine IL-4, IL-8, IL-10, and TNF-α Levels Correlate with Pulmonary Function in Patients with Asthma-Chronic Obstructive Pulmonary Disease (COPD) Overlap Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Two ST11Gut microbesArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveLung contusion injury produces a vulnerable window within the inflammatory defenses of the lung that predisposes the patient to pneumonia. Interleukin 10 (IL-10) is a known anti-inflammatory mediator produced by macrophages and capable of downregulating acute lung inflammation. We investigated the impact of increased levels of IL-10 within the lung on survival and the host response to trauma in the setting of lung contusion (LC) and gram-negative pneumonia.
designA bitransgenic, tetracycline-inducible, lung-specific human IL-10 overexpression (IL-10 OE) mouse model and single transgenic (TG-) control mice were used. Mice underwent LC injury or sham injury (sham) at time -6 h. At time 0, animals were inoculated intratracheally with 500 colony-forming units of Klebsiella pneumoniae (pneu). Bronchoalveolar lavage fluid, lung tissue specimens, or purified macrophages were collected. Lung tissue and blood bacteria levels were quantified. Cytokine levels were assayed by enzyme-linked immunosorbent assay, and gene expression levels were evaluated by real-time polymerase chain reaction. Cell-type identification and quantification were done using real-time polymerase chain reaction and flow cytometry. MAIN
resultsInterleukin 10 OE mice demonstrated decreased 5-day survival compared with TG- mice following LC + pneu (0 vs. 30%, P < 0.0001). Interleukin 10 OE mice had significantly higher lung bacteria counts (P = 0.02) and levels of bacteremia (P = 0.001) at 24 h. The IL-10 OE mice recruited more neutrophils into the alveoli as measured in bronchoalveolar lavage fluid compared with TG- mice. Alveolar macrophages from IL-10 OE mice displayed increased alternative activation (M2 macrophages, P = 0.046), whereas macrophages from TG- mice exhibited classic activation (M1 macrophages) and much higher intracellular bacterial killing potential (P = 0.03). Interleukin 6, keratinocyte-derived chemokine, and macrophage inflammatory protein 2 levels were significantly elevated in IL-10 OE LC + pneu animals (P < 0.05).
conclusionsLung-specific IL-10 overexpression induces alternative activation of alveolar macrophages. This shift in macrophage phenotype decreases intracellular bacterial killing, resulting in a more pronounced bacteremia and accelerated mortality in a model of LC and pneumonia.
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