Interactions of Pneumocystis with Alveolar Macrophages and Epithelial Cells

2004 ◽  
pp. 249-272
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages

scholarly journals Lung macrophages drive mucus production and steroid-resistant inflammation in chronic bronchitis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Kristina Andelid ◽  
Karolina Öst ◽  
Anders Andersson ◽  
Esha Mohamed ◽  
Zala Jevnikar ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Bronchitis ◽  
Cross Talk ◽  
Alveolar Macrophages ◽  
Ex Vivo ◽  
Bronchial Epithelial Cells ◽  
Steroid Resistance ◽  
Bronchial Epithelial ◽  
Steroid Resistant ◽  
Copd Patients

Abstract Background Patients with chronic obstructive pulmonary disease (COPD) frequently suffer from chronic bronchitis (CB) and display steroid-resistant inflammation with increased sputum neutrophils and macrophages. Recently, a causal link between mucus hyper-concentration and disease progression of CB has been suggested. Methods In this study, we have evaluated the steroid sensitivity of purified, patient-derived sputum and alveolar macrophages and used a novel mechanistic cross-talk assay to examine how macrophages and bronchial epithelial cells cross-talk to regulate MUC5B production. Results We demonstrate that sputum plug macrophages isolated from COPD patients with chronic bronchitis (COPD/CB) are chronically activated and only partially respond to ex vivo corticosteroid treatment compared to alveolar macrophages isolated from lung resections. Further, we show that pseudo-stratified bronchial epithelial cells grown in air–liquid-interface are inert to direct bacterial lipopolysaccharide stimulation and that macrophages are able to relay this signal and activate the CREB/AP-1 transcription factor complex and subsequent MUC5B expression in epithelial cells through a soluble mediator. Using recombinant protein and neutralizing antibodies, we identified a key role for TNFα in this cross-talk. Conclusions For the first time, we describe ex vivo pharmacology in purified human sputum macrophages isolated from chronic bronchitis COPD patients and identify a possible basis for the steroid resistance frequently seen in this population. Our data pinpoint a critical role for chronically activated sputum macrophages in perpetuating TNFα-dependent signals driving mucus hyper-production. Targeting the chronically activated mucus plug macrophage phenotype and interfering with aberrant macrophage-epithelial cross-talk may provide a novel strategy to resolve chronic inflammatory lung disease.

scholarly journals Azithromycin increases phagocytosis of apoptotic bronchial epithelial cells by alveolar macrophages

2006 ◽  
Vol 28 (3) ◽  
pp. 486-495 ◽  
Author(s):  
S. Hodge ◽  
G. Hodge ◽  
S. Brozyna ◽  
H. Jersmann ◽  
M. Holmes ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Pseudomonas aeruginosa LPS or Flagellin Are Sufficient to Activate TLR-Dependent Signaling in Murine Alveolar Macrophages and Airway Epithelial Cells

PLoS ONE ◽  
2009 ◽  
Vol 4 (10) ◽  
pp. e7259 ◽  
Author(s):  
Eloïse Raoust ◽  
Viviane Balloy ◽  
Ignacio Garcia-Verdugo ◽  
Lhousseine Touqui ◽  
Reuben Ramphal ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

scholarly journals Effect of exposure to silica on human alveolar macrophages in supporting growth activity in type II epithelial cells.

Thorax ◽  
1996 ◽  
Vol 51 (8) ◽  
pp. 781-786 ◽  
Author(s):  
B. Melloni ◽  
O. Lesur ◽  
T. Bouhadiba ◽  
A. Cantin ◽  
M. Martel ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Type Ii ◽  
Human Alveolar Macrophages ◽  
Growth Activity

scholarly journals Characterization of Early Stages of Human Alveolar Infection by the Q Fever AgentCoxiella burnetii

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Amanda L. Dragan ◽  
Richard C. Kurten ◽  
Daniel E. Voth
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Human Lung ◽  
Q Fever ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Human Lung Tissue ◽  
Content Type ◽  
Alveolar Epithelial

ABSTRACTHuman Q fever is caused by the intracellular bacterial pathogenCoxiella burnetii. Q fever presents with acute flu-like and pulmonary symptoms or can progress to chronic, severe endocarditis. After human inhalation,C. burnetiiis engulfed by alveolar macrophages and transits through the phagolysosomal maturation pathway, resisting the acidic pH of lysosomes to form a parasitophorous vacuole (PV) in which to replicate. Previous studies showed thatC. burnetiireplicates efficiently in primary human alveolar macrophages (hAMs) inex vivohuman lung tissue. AlthoughC. burnetiireplicates in most cell typesin vitro, the pathogen does not grow in non-hAM cells of human lung tissue. In this study, we investigated the interaction betweenC. burnetiiand other pulmonary cell types apart from the lung environment.C. burnetiiformed a prototypical PV and replicated efficiently in human pulmonary fibroblasts and in airway, but not alveolar, epithelial cells. Atypical PV expansion in alveolar epithelial cells was attributed in part to defective recruitment of autophagy-related proteins. Further assessment of theC. burnetiigrowth niche showed that macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response toC. burnetiiand ultimately shifted to an M2-polarized phenotype characteristic of anti-inflammatory macrophages. Considering our findings together, this study provides further clarity on the uniqueC. burnetii-lung dynamic during early stages of human acute Q fever.

Ozone-induced release of cytokines and fibronectin by alveolar macrophages and airway epithelial cells

1994 ◽  
Vol 266 (6) ◽  
pp. L612-L619 ◽  
Author(s):  
R. B. Devlin ◽  
K. P. McKinnon ◽  
T. Noah ◽  
S. Becker ◽  
H. S. Koren
Keyword(s):  
Epithelial Cells ◽  
Cell Line ◽  
Alveolar Macrophages ◽  
Airway Epithelial Cells ◽  
Airway Hyperreactivity ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelial Cells

Acute exposure of animals and humans to ozone results in decrements in lung function, development of airway hyperreactivity, inflammation, edema, damage to pulmonary cells, and production of several compounds with tissue damaging, fibrinogenic or fibrotic potential. The contribution of airway epithelial cells and alveolar macrophages to these processes is unclear. In this study we have directly exposed human alveolar macrophages and human airway epithelial cells to ozone in vitro and measured the cytotoxic effects of ozone, as well as the production of the inflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8), and fibronectin, all of which are substantially elevated in the bronchoalveolar lavage fluid of humans exposed to ozone. Cells were grown on rigid, collagen-impregnated filter supports, and the interaction of cells with ozone facilitated by exposing them to the gas with medium below the support but no medium on top of the cells. The results show that, although macrophages are much more sensitive to ozone than epithelial cells, they do not produce increased amounts of IL-6, IL-8, or fibronectin following ozone exposure. In contrast, epithelial cells produce substantially more of all three proteins following ozone exposure, and both IL-6 and fibronectin are secreted vectorially. An immortalized human airway epithelial cell line (BEAS 2B) was used in these experiments since human airway epithelial cells are infrequently available for in vitro studies. Data from this study extend previous findings which suggest that the BEAS cell line is a useful model to study the interaction between airway epithelial cells and environmental toxicants.

Pneumonia in Lambs Inoculated with Bordetella parapertussis: Bronchoalveolar Lavage and Ultrastructural Studies

1988 ◽  
Vol 25 (4) ◽  
pp. 297-303 ◽  
Author(s):  
W. Chen ◽  
M. R. Alley ◽  
B. W. Manktelow ◽  
D. Hopcroft ◽  
R. Bennett
Keyword(s):  
Epithelial Cells ◽  
Bronchoalveolar Lavage ◽  
Alveolar Macrophages ◽  
Bronchial Epithelium ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Bordetella Parapertussis ◽  
Alveolar Epithelial ◽  
Ultrastructural Studies ◽  
Cell Counts

Eight colostrum-deprived lambs were inoculated intratracheally with ovine isolates of Bordetella parapertussis. Fluids obtained by bronchoalveolar lavage had a large increase in total cell counts 24 hours after inoculation; up to 93% of cells were neutrophils. From 3 days after inoculation, the number of alveolar macrophages in lavage samples was markedly increased. From 5 days onwards, many alveolar macrophages had moderate to severe cytoplasmic vacuolation. Topographically, tracheal and bronchial epithelium was covered by a large amount of inflammatory exudate 24 hours after inoculation. Later, the tracheobronchial epithelium showed focal extrusions from ciliated cells, which were occasionally associated with B. parapertussis organisms. Ultrastructurally, cytopathological changes associated with B. parapertussis infection were mild focal degeneration of airway epithelium with slight loss of cilia, moderate to severe degeneration of type I and type II alveolar epithelial cells, and focal inflammation in the lungs. These results suggest that the primary targets of B. parapertussis infection are alveolar macrophages and the epithelial cells of bronchioles and alveoli.

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