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 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.

Human lung cell beta 2-adrenergic receptors desensitize in response to in vivo administered beta-agonist

1995 ◽  
Vol 269 (5) ◽  
pp. L709-L714 ◽  
Author(s):  
J. Turki ◽  
S. A. Green ◽  
K. B. Newman ◽  
M. A. Meyers ◽  
S. B. Liggett
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Adrenergic Receptors ◽  
Cell Types ◽  
Bronchial Epithelial Cells ◽  
Beta Agonist ◽  
Target Tissue ◽  
Camp Accumulation ◽  
Bronchial Epithelial ◽  
Beta 2

Few studies have addressed whether target tissue adrenergic receptors in humans undergo desensitization in response to agonist administration. To determine whether lung cell beta 2-adrenergic receptors (beta 2-AR) undergo such desensitization, we harvested bronchial epithelial cells and alveolar macrophages via bronchoscopy from eight normal subjects before and after inhalation of six doses of the beta-agonist metaproterenol given over 24 h. After metaproterenol inhalation, beta 2-AR expression as determined by 125I-labeled cyanopindolol binding decreased approximately 70% on bronchial epithelial cells, from 6.3 +/- 0.7 to 2.0 +/- 0.2 fmol/mg (P < 0.001) and to a similar extent on macrophages from 13.3 +/- 0.4 to 3.9 +/- 0.6 fmol/mg (P < 0.001). Agonist inhalation also resulted in impairment of beta 2-AR function in both cell types. With bronchial epithelial cells, maximal isoproterenol-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation decreased from 9.5 +/- 1.8 to 4.9 +/- 1.2 pmol/10(6) cells (P = 0.003), which amounts to a 48 +/- 6% desensitization. Isoproterenol-stimulated cAMP accumulation in alveolar macrophages decreased from 39.5 +/- 9.0 to 2.9 +/- 0.3 pmol/10(6) cells (P = 0.007), equivalent to 86 +/- 5% desensitization. The cAMP response to forskolin in both cell types was unaffected by metaproterenol inhalation. Thus administration of inhaled beta-agonists results in substantial downregulation and functional desensitization of lung cell beta 2-AR. This supports the concept of a dynamically regulated beta 2-AR in humans, the function of which can be attenuated in relevant target tissues by administration of standard doses of beta-agonist.

scholarly journals Exosomal miR-380 derived from alveolar macrophages in COPD is involved in enhanced proliferation of human bronchial epithelial cells

2020 ◽  
Author(s):  
Yunxin Fan ◽  
Xiumin Feng ◽  
Jingxi Zhang ◽  
Chong Bai
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Proliferative Activity ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Tnf Α ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Chronic obstructive pulmonary disease (COPD) is closely related to the occurrence of lung cancer. Both diseases involve changes in the biological function and structure of bronchial epithelial cells. Recently, the role of exosomes in intercellular communication has attracted increasing attention from researchers. As an important molecule carried by exosomes, the role of exosomal miRNAs in diseases such as COPD and lung cancer has also been gradually confirmed. The aim of this study is to investigate the effect of exosomal miRNA derived from macrophages on the proliferation of bronchial epithelial cells. Results After co-culture with alveolar macrophages from COPD, the proliferative activity and migration capacity of 16HBE was significantly enhanced compared with those from healthy controls. Alveolar macrophages from COPD promoted the production of MUC5AC, MUC5B and MUC2 as well as TNF - α and IL-6 in 16HBE. MiR-380 was up-regulated miRNA in exosomes derived from alveolar macrophages through miRNA array analysis. Exosomal miR-380 enhanced the proliferation and migration of 16HBE, promoted the expression of mucins such as MUC5AC, MUC5B and MUC2 of 16HBE, but inhibited the expression of CFTR protein. The target gene of miR-380 was CFTR. The proliferative activity and migration ability of 16HBE was enhanced by blocking CFTR. Conclusions Alveolar macrophages from COPD can enhance the proliferation and migration of 16HBE and promote the expression of mucin and proinflammatory mediators such as IL-6 and TNF-α. Exosomal miR-380 derived from macrophages in COPD was significantly up-regulated. The enhancement of proliferation and migration may be related to the down regulation of CFTR by exosomes delivering miR-380 to bronchial epithelial cells, opening a new way for the therapy and prevention in COPD and its complication.

scholarly journals Microscopic and bacteriological comparison of paired sputa and transtracheal aspirates

1977 ◽  
Vol 6 (4) ◽  
pp. 396-399
Author(s):  
R W Geckler ◽  
D H Gremillion ◽  
C K McAllister ◽  
C Ellenbogen
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Bacterial Pneumonia ◽  
Diagnostic Value ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Potential Pathogen ◽  
Group 5

Ninety-six sputum specimens from patiens with pneumonia were microscopically screened for leukocytes and buccal squamous epithelial (BSE) cells. Cultures of these specimens were compared with cultures of paired transtracheal aspirates (TTA). Agreement between sputa with less than 25 BSE cells per 100X field and TTA was good (79%). Only 27% of the specimens with greater than 25 BSE cells per 100X field agreed with TTA. Sixty-six of the sputa were of group 5 quality, i.e., greater than 25 leukocytes and less than 10 BSE cells per 100X field. A potential pathogen growing in one of these specimens was 94% predictive of growth in the TTA. If a group 5 sputum was negative for a potential pathogen, there was a 45% chance that a fastidious organism had been overgrown or overlooked. The presence of definite lower tract secretions in group 5 sputa as determined by visualizing bronchial epithelial cells and alveolar macrophages did not significantly increase the diagnostic value of these specimens. Microscopic screening of sputum before culture with rejection of selected specimens can increase the value of sputum in determining the etiology of bacterial pneumonia.

Effect of Atorvastatin on PM10-induced Cytokine Production by Human Alveolar Macrophages and Bronchial Epithelial Cells

2009 ◽  
Vol 28 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Noriho Sakamoto ◽  
Shizu Hayashi ◽  
Hiroshi Mukae ◽  
Renaud Vincent ◽  
James C. Hogg ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Air Pollution ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Alveolar Macrophages ◽  
Messenger Rna ◽  
Cytokine Production ◽  
Ambient Air ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Exposure to ambient air pollution particles (PM10) has been associated with increased cardiovascular morbidity and mortality. Inhaled pollutants induce a pulmonary and systemic inflammatory response that is thought to exacerbate cardiovascular disease. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to have anti-inflammatory effects that could contribute to their beneficial effect in cardiovascular disease. The aim of this study is to determine the effects of statins on PM10-induced cytokine production in human bronchial epithelial cells (HBECs) and alveolar macrophages (AMs). Primary HBECs and AMs are obtained from resected human lung. Cells are pretreated with different concentrations of atorvastatin for 24 hours and then exposed to 100 μg/mL urban air pollution particles (EHC-93). Cytokine levels (interleukin-1β, interleukin-8, granulocyte-macrophage colonystimulating factor, interleukin-6, and tumor necrosis factor-α) are measured at messenger RNA and protein levels using real-time polymerase chain reaction and bead-based multiplex immunoassay, respectively. PM10 exposure increases production of these cytokines by both cell types. Atorvastatin attenuates PM10-induced messenger RNA expression and cytokine production by AMs but not by HBECs. It is concluded that statins can modulate the PM10-induced inflammatory response in the lung by reducing mediator production by AMs.

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