A comparison of alveolar macrophages and pulmonary surfactant(?) Obtained from the lungs of human smokers and nonsmokers by endobronchial lavage

Pratt, S. A.; Finley, Theodore N.; Smith, Morris H.; Ladman, Aaron J.

doi:10.1002/ar.1091630402

Cited by 89 publications

(31 citation statements)

References 24 publications

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“…More than 90% of surfactant lipids are phospholipids [16] and cigarette smoke's deleterious effects on surfactant has been described as early as the 1960s and 1970s [3,6]. Hence, damaged surfactant lipids are, in our view, the most likely source.…”

Section: Figurementioning

confidence: 88%

“…Cigarette smoke's damaging effect on surfactant lipids was initially proposed in the late 1960s and 1970s [3,6]. Moreover, our group recently observed the conserved induction of genes involved in lipid metabolism by cigarette smoke in the lungs of both humans and mice [7].…”

Section: Introductionmentioning

confidence: 92%

“…One of the most striking features associated with smoking is the increase in size and complexity of the pulmonary macrophage [2,3], a critical immune sentinel [4] and key player in the catabolism of damaged surfactant [5]. Cigarette smoke's damaging effect on surfactant lipids was initially proposed in the late 1960s and 1970s [3,6].…”

Section: Introductionmentioning

confidence: 99%

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Disruption of pulmonary lipid homeostasis drives cigarette smoke-induced lung inflammation in mice

et al. 2015

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Overwhelming evidence links inflammation to the pathogenesis of smoking-related pulmonary diseases, especially chronic obstructive pulmonary disease (COPD). Despite an increased understanding of the disease pathogenesis, mechanisms initiating smoking-induced inflammatory processes remain incompletely understood.To investigate the mechanisms that initiate and propagate smoke-induced inflammation, we used a wellcharacterised mouse model of cigarette smoke exposure, mice deficient for interleukin (IL)-1α, IL-1β and Toll-like receptor 4, and antibodies blocking granulocyte-macrophage colony-stimulating factor (GM-CSF). Studies were also pursued using intranasal delivery of human oxidised low-density lipoprotein (hOxLDL), a source of oxidised lipids, to investigate the inflammatory processes associated with impaired lipid homeostasis.We found that cigarette smoke exposure rapidly led to lipid accumulation in pulmonary macrophages, a defining feature of foam cells, which in turn released high levels of IL-1α. In smoke-exposed IL-1α-deficient mice, phospholipids accumulated in the bronchoalveolar lavage, a phenomenon also observed when blocking GM-CSF. Intranasal administration of hOxLDL led to lipid accumulation in macrophages and initiated an inflammatory process that mirrored the characteristics of cigarette smoke-induced inflammation.These findings identify a link between lipid accumulation in macrophages, inflammation and damaged surfactant, suggesting that the response to damaged pulmonary surfactant is a central mechanism that drives cigarette smoke-induced inflammation. Further investigations are required to explore the role of distorted lipid homeostasis in the pathogenesis of COPD. @ERSpublications Lipid accumulation in pulmonary macrophages drives cigarette smoke-induced lung inflammation

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Section: Figurementioning

confidence: 88%

Section: Introductionmentioning

confidence: 92%

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Disruption of pulmonary lipid homeostasis drives cigarette smoke-induced lung inflammation in mice

et al. 2015

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“…AMs from human smokers ultrastructurally differ from those of nonsmokers; they are larger [8,13], contain more cell organelles, pseudopodia [8,14] and several inclusions ("smokers inclusions") [6,7,15,16]. The heterogeneity seems to be more pronounced in AMs of smokers than nonsmokers, as indicated by differences in their light scattering and autofluorescent properties [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the AMs of smokers are generally larger and contain more cytoplasmic inclusions [6][7][8], and they appear to constitute a morphologically and functionally heterogenous cell population.…”

Section: DI If Ff Fe Er Re En Nt T F Fu Un Nc Ct Ti Io On Na Al L Amentioning

confidence: 99%

Different functional and morphological characteristics in a nonadherent subpopulation of human macrophages recovered by bronchoalveolar lavage

Sköld¹,

Barck²,

Lundahl³

et al. 1995

Eur Respir J

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D Di if ff fe er re en nt t f fu un nc ct ti io on na al l aan nd d m mo or rp ph ho ol lo og gi ic ca al l c ch ha ar ra ac ct te er ri is st ti ic cs s i in n a a n no on na ad dh he er re en nt t s su ub bp po op pu ul la at ti io on n o of f h hu um ma an n m ma ac cr ro op ph ha ag ge es s r re ec co ov ve er re ed d b by y b br ro on nc ch ho oa al lv ve eo ol la ar r l la av va ag ge e ABSTRACT: The alveolar macrophages (AMs) constitute a morphologically and functionally heterogenous cell population. The adhesive properties of these cells are important for their role in host defence. To focus on the heterogeneity, a population of nonadherent macrophages were characterized functionally and morphologically. These cells were then compared with the total alveolar macrophage population. Alveolar cells (>95% alveolar macrophages), were recovered by bronchoalveolar lavage (BAL) from healthy smokers. Nonadherent macrophages were separated by adhesion. The phagocytic capacity and the autofluorescent properties of the cell populations were determined in flow cytofluorometric assays. In addition, electron microscopic evaluation was performed.The alveolar macrophage adhesion to wells coated with albumin increased in a time-dependent manner. After 15 min, median 47%, interquartile range 42-52% (uncoated wells 68%, 67-72%) of the alveolar macrophages were attached; and after 60 min, 56%, 51-58% (uncoated wells 73%, 71-76%) of the alveolar macrophages were attached. The nonadherent alveolar macrophage population had less phagocytic capacity. The cell autofluorescence increased with increasing cell size and cell complexity/granularity in both populations. The nonadherent cells were more autofluorescent, indicating an increased granularity/complexity. These findings were confirmed with electron microscopy. Thus, the nonadherent alveolar macrophages had more cytoplasmic inclusions than the total alveolar macrophage population (volume density median 0.39, interquartile range 0.35-0.46 and 0.31, 0.26-0.34, respectively), but less surface protusions.We conclude that in lavage fluid from human smokers there is an ultrastructurally specific subpopulation of alveolar macrophages, showing less adhesive properties and impaired phagocytic capacity in vitro. These macrophages may be older alveolar cells or, alternatively, airway macrophages. Since only alveolar macrophages from smokers were investigated, we cannot draw any conclusions regarding alveolar cells from nonsmokers. Nevertheless, the heterogeneity of the lavaged cells should be taken into consideration when the functional ability of the alveolar macrophages are evaluated.

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Properties of Alveolar Cells and Tissues That Strengthen Alveolar Defenses

Sorokin¹

1970

Arch Intern Med

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A comparison of alveolar macrophages and pulmonary surfactant(?) Obtained from the lungs of human smokers and nonsmokers by endobronchial lavage

Cited by 89 publications

References 24 publications

Disruption of pulmonary lipid homeostasis drives cigarette smoke-induced lung inflammation in mice

Disruption of pulmonary lipid homeostasis drives cigarette smoke-induced lung inflammation in mice

Different functional and morphological characteristics in a nonadherent subpopulation of human macrophages recovered by bronchoalveolar lavage

Properties of Alveolar Cells and Tissues That Strengthen Alveolar Defenses

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