In Vitro Toxicity of Tobacco Smoke Solutions to Rabbit Alveolar Macrophages

Rs, Stuart; Wh, Higgins; Pw, Brown

doi:10.1080/00039896.1978.10667323

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…The apoptosis induced in these models was related to an increase in oxidative stress, Bax protein accumulation, mitochondrial dysfunction, and mitochondrial cytochrome c release, but was unrelated to p53, Fas, and caspase activation [142]. CS extract (CSE) led to apoptosis at a lower density (10% to 25%) but to cell death and necrosis at higher density (50% to 100%) [143], confirmed by earlier in vitro studies [144,145]. Machiya and co-workers reported that CS-induced apoptosis in LM was partly dependent on caspase-3, in contrast to the reports of Aoshiba [142].…”

Section: Lm Apotosis Accociated With Cigarette Smoke Exposuresupporting

confidence: 65%

Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease

Akata

Eeden

2020

IJMS

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Chronic obstructive pulmonary disease (COPD) is caused by the chronic exposure of the lungs to toxic particles and gases. These exposures initiate a persistent innate and adaptive immune inflammatory response in the airways and lung tissues. Lung macrophages (LMs) are key innate immune effector cells that identify, engulf, and destroy pathogens and process inhaled particles, including cigarette smoke and particulate matter (PM), the main environmental triggers for COPD. The number of LMs in lung tissues and airspaces is increased in COPD, suggesting a potential key role for LMs in initiating and perpetuating the chronic inflammatory response that underpins the progressive nature of COPD. The purpose of this brief review is to discuss the origins of LMs, their functional properties (chemotaxis, recruitment, mediator production, phagocytosis and apoptosis) and changes in these properties due to exposure to cigarette smoke, ambient particulate and pathogens, as well as their persistent altered functional properties in subjects with established COPD. We also explore the potential to therapeutically modulate and restore LMs functional properties, to improve impaired immune system, prevent the progression of lung tissue destruction, and improve both morbidity and mortality related to COPD.

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Section: Lm Apotosis Accociated With Cigarette Smoke Exposuresupporting

confidence: 65%

Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease

Akata

Eeden

2020

IJMS

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“…At room temperature, aqueous smoke solution (tobacco smoke extract) was prepared by putting the smoke from a cigarette through phosphate‐buffered saline as described previously (23). The smoke solution was collected and then adjusted to a pH of 7.4 with sodium bicarbonate water and filtered through a 0.22 µm filter (Millipore Co., Bedford, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

Tobacco smoke extract induces age‐related changes due to modulation of TGF‐β

Yin

Morita

Tsuji

2003

Experimental Dermatology

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We have recently shown that tobacco smoking, like ultraviolet A radiation, is an important factor contributing to premature skin aging. We found that tobacco smoke extract decreased type I and III procollagen, increased tropoelastin mRNA, and induced abnormal accumulation of proteoglycans and matrix metalloproteinase (MMP)-1 and MMP-3 in cultured skin fibroblasts. This indicated that common molecular features might underlie the premature aging of the skin induced by tobacco smoke extract, including abnormal regulation of extracellular matrix deposition through elevated MMPs, reduced collagen production, abnormal tropoelastin accumulation, and altered proteoglycans. With the exception that reactive oxygen species were mediated in the aging process, transforming growth factor (TGF)-beta1 was found to play a crucial role in the age-related alterations induced by tobacco smoke extract. Here we report that tobacco smoke extract blocks cellular responsiveness to TGF-beta1 through the induction of a non-functional latent form of TGF-beta1, and downregulation of the TGF-beta1 receptor. This paper shows the evidence for the role of tobacco smoking in skin aging and describes how modulation of TGF-beta1 levels might retard premature skin aging.

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“…CS is also known to be toxic to AMs. In in vitro studies, acute CS exposure has been shown to kill AMs (31,35), although the type of cell death, i.e., necrosis or apoptosis, remains uncertain. The mechanism of CS toxicity to AMs may involve oxidative stress, an important mediator of cell death via both necrosis and apoptosis.…”

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confidence: 99%

Acute cigarette smoke exposure induces apoptosis of alveolar macrophages

Aoshiba

Tamaoki

Nagai

2001

American Journal of Physiology-Lung Cellular and Molecular Phys

191

127

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Alveolar macrophages (AMs) may play a critical role in cigarette smoke (CS)-related pulmonary diseases. This study was designed to determine whether CS induces apoptosis of AMs. In in vitro studies, mouse, rat, and human AMs and human blood monocyte-derived macrophages cultured with aqueous whole CS extracts underwent apoptosis that was detected by light and electron microscopy and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. The gas phase of CSE did not cause apoptosis. The CS-induced apoptosis was associated with increased oxidative stress, Bax protein accumulation, mitochondrial dysfunction, and mitochondrial cytochrome c release but was independent of p53, Fas, and caspase activation. This apoptosis was inhibited by antioxidants such as glutathione, ascorbic acid, and alpha-tocopherol. In in vivo studies where rats were exposed to the smoke from 10 cigarettes over 5 h in an exposure chamber, approximately 3% of AMs obtained by bronchoalveolar lavage after 24 h showed apoptosis. These results suggest that acute CS exposure is capable of inducing apoptosis of AMs.

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In Vitro Toxicity of Tobacco Smoke Solutions to Rabbit Alveolar Macrophages

Cited by 7 publications

References 15 publications

Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease

Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease

Tobacco smoke extract induces age‐related changes due to modulation of TGF‐β

Acute cigarette smoke exposure induces apoptosis of alveolar macrophages

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