The inflammatory response in humans after inhalation of bacterial endotoxin: a review

Thorn, Jörgen

doi:10.1007/s000110050751

Cited by 205 publications

(154 citation statements)

References 45 publications

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“…By binding to toll-like-receptor-4 (TLR-4), LPS can activate the NF-κB signaling pathway, and this leads to induction of many genes involved in inflammation, including the expression of various chemokines. LPS inhalation has been used as a model for inflammation of the lung (18). LPS-induced inflammatory responses include systemic effects such as fever and granulocytosis in blood and local effects such as an increase of cytokines in sputum and influx of leukocytes (18) and, in the mouse model, an LPS-induced influx of small macrophages has been documented (19).…”

Section: Chemokine Expression By Small Sputum Macrophages In Copdmentioning

confidence: 99%

“…LPS inhalation has been used as a model for inflammation of the lung (18). LPS-induced inflammatory responses include systemic effects such as fever and granulocytosis in blood and local effects such as an increase of cytokines in sputum and influx of leukocytes (18) and, in the mouse model, an LPS-induced influx of small macrophages has been documented (19). We can demonstrate herein that LPS targeted to the airways of the lung (Moeller et al, submitted) will lead to an influx of small macrophages.…”

Section: Chemokine Expression By Small Sputum Macrophages In Copdmentioning

confidence: 99%

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Chemokine Expression by Small Sputum Macrophages in COPD

Frankenberger

Eder

Hofer

et al. 2011

Mol Med

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Small sputum macrophages represent highly active cells that increase in the airways of patients with inflammatory diseases such as chronic obstructive pulmonary disease (COPD). It has been reported often that levels of cytokines, chemokines and proteases are increased in sputum supernatants of these patients. In COPD, the small sputum macrophages may contribute to these supernatant proteins and recruit additional cells via specific chemokine expression patterns. We therefore investigated the expression profile of chemokines in sputum macrophages obtained from COPD patients in comparison to cells from healthy donors and cells isolated after inhalation of lipopolysaccharide (LPS). We used the minimally invasive procedure of sputum induction and have purified macrophages with the RosetteSep technology. Using macrophage purification and flow cytometry we show that in COPD small sputum macrophages account for 85.9% ± 8.3% compared with 12.9% ± 7.1% of total macrophages in control donors. When looking at chemokine expression we found, for the small macrophages in COPD, increased transcript and protein levels for CCL2, CCL7, CCL13 and CCL22 with a more than 100-fold increase for CCL13 mRNA (P < 0.001). Looking at active smokers without COPD, there is a substantial increase of small macrophages to 60% ± 15% and, here, chemokine expression is increased as well. In a model of airway inflammation healthy volunteers inhaled 20 μg of lipopolysaccharide (LPS), which resulted in an increase of small sputum macrophages from 18% ± 19% to 64% ± 25%. The pattern of chemokine expression was, however, different with an upregulation for CCL2 and CCL7, while CCL13 was downregulated three-fold in the LPS-induced small macrophages. These data demonstrate that sputum macrophages in COPD show induction of a specific set of CCL chemokines, which is distinct from what can be induced by LPS.

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Section: Chemokine Expression By Small Sputum Macrophages In Copdmentioning

confidence: 99%

Section: Chemokine Expression By Small Sputum Macrophages In Copdmentioning

confidence: 99%

Chemokine Expression by Small Sputum Macrophages in COPD

Frankenberger

Eder

Hofer

et al. 2011

Mol Med

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“…Shower aerosol particles can be sufficiently small to carry bacteria deep into the airways (1). Pulmonary disease and other health risks such as asthma, bronchitis, and hypersensitivity pneumonitis are associated with inhalation of both viable bacteria and inviable microorganisms or their components (2)(3)(4). It has been hypothesized that the rise in pulmonary infections by nontuberculous mycobacteria (NTM) over recent decades is linked to increased use of showers rather than baths (5).…”

mentioning

confidence: 99%

Opportunistic pathogens enriched in showerhead biofilms

Feazel

Baumgartner²,

Peterson³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

495

364

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The environments we humans encounter daily are sources of exposure to diverse microbial communities, some of potential concern to human health. In this study, we used culture-independent technology to investigate the microbial composition of biofilms inside showerheads as ecological assemblages in the human indoor environment. Showers are an important interface for human interaction with microbes through inhalation of aerosols, and showerhead waters have been implicated in disease. Although opportunistic pathogens commonly are cultured from shower facilities, there is little knowledge of either their prevalence or the nature of other microorganisms that may be delivered during shower usage. To determine the composition of showerhead biofilms and waters, we analyzed rRNA gene sequences from 45 showerhead sites around the United States. We find that variable and complex, but specific, microbial assemblages occur inside showerheads. Particularly striking was the finding that sequences representative of non-tuberculous mycobacteria (NTM) and other opportunistic human pathogens are enriched to high levels in many showerhead biofilms, >100-fold above background water contents. We conclude that showerheads may present a significant potential exposure to aerosolized microbes, including documented opportunistic pathogens. The health risk associated with showerhead microbiota needs investigation in persons with compromised immune or pulmonary systems.bioaerosols ͉ Mycobacterium avium complex ͉ Non-tuberculous mycobacteria ͉ public health ͉ rRNA metagenomics

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“…1-5.0 |Lig/ml) in the causative water (13,14). Endotoxin is an extremely potent agent of lung injury and the inhalation of endotoxin can cause symptomssuch as chills and fever, a decrease in DLC0, an increase in airway hyperresponsiveness, and increases in neutrophils as well as lymphocytes in BALand blood, in a dose-dependent fashion (16,17). Bacterial endotoxins and fungal toxins have also been proposed as causative agents of organic dust toxic syndrome (ODTS) (3).…”

Section: Discussionmentioning

confidence: 99%

Humidifier Lung: Possible Contribution of Endotoxin-induced Lung Injury.

et al. 2002

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A 56-year-old man was admitted with cough, fever, myalgia, and arthralgia. Chest computed tomography demonstrated bilateral diffuse ground-glass opacities predominantly in the upper lungs. Subpleural non-segmental consolidation was observed in the late phase. Hypersensitivity pneumonitis was suspected, and an environmental provocation test with the incidental use of a home ultrasonic humidifier was positive. Unlike typical hypersensitivity pneumonitis, serum KL-6 levels were normal. Although several microorganisms were isolated from the humidifier water, there was no evidence for immunesensitization. Wedetected high amounts of endotoxin in the humidifier water, which mayhave contributed to the lung injury of this patient.

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The inflammatory response in humans after inhalation of bacterial endotoxin: a review

Cited by 205 publications

References 45 publications

Chemokine Expression by Small Sputum Macrophages in COPD

Chemokine Expression by Small Sputum Macrophages in COPD

Opportunistic pathogens enriched in showerhead biofilms

Humidifier Lung: Possible Contribution of Endotoxin-induced Lung Injury.

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