Decreased Leukocyte Deformability after Acute Cigarette Smoking in Humans

Drost, Ellen; Selby, C.; Bridgeman, M.M.E.; MacNee, William

doi:10.1164/ajrccm/148.5.1277

Cited by 46 publications

(17 citation statements)

References 32 publications

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“…20 The mechanisms related to this phenomenon are not completely understood, but may involve activation of adhesion molecules, changes in leukocyte cytoskeletons, and local hemodynamic disorders. [20][21][22] Whatever the mechanisms involved, the acute elevation of H 2 O 2 -E levels found in this study reflect ROS respiratory overloading secondary to the smoking habit.…”

Section: Discussionmentioning

confidence: 71%

Increased exhalation of hydrogen peroxide in healthy subjects following cigarette consumption

et al. 2000

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Section: Discussionmentioning

confidence: 71%

Increased exhalation of hydrogen peroxide in healthy subjects following cigarette consumption

et al. 2000

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“…CS exposure has been shown by immunogold electron microscopy to induce the upregulation of P32-integrin adhesion molecules on leukocytes sequestered in the upper lobes of rabbit lungs (31), to reduce leukocyte deformability (43), and to increase in rats and humans the production by endothelial cells of proaggregatory thromboxane while at the same time inhibiting the generation of antiaggregatory prostacyclin (30). Whether these effects of CS are ROS-dependent and could thus be affected by vitamin C remains to be shown.…”

Section: Resultsmentioning

confidence: 99%

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Lehr¹,

Frei²,

Arfors³

1994

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

153

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A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro-and macrovascular endothelium. A previous study, using a skinfold chamber model for intravial fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro-and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 ± 11.0 vs. 149.6 ± 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 ± 4.2 vs. 54.3 ± 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 ± 0.4 vs. 12.4 ± 5.6 leukocytes per mm2 P < 0.01; means ± SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CSinduced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 ± 22.2 spM, n 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.Cigarette smoke (CS) has been identified as an independent major risk factor for the development of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease, emphysema, atherosclerosis, and coronary artery disease (1). Although the spectrum of adverse effects of CS involves multiple tissue and organ systems, a feature common to the pathomechanism of most CS-associated diseases is the activation and adhesion of circulating leukocytes to micro-and/or macrovascular endothelium (2-4), followed by acute and/or chronic leukocyte-mediated tissue damage (5, 6). In agreement with earlier reports on the sequestration and activation of leukocytes in the pulmonary microcirculation in rabbits (7), hamsters (8, 9), and humans (10), intravital microscopy in a skinfold chamber model in hamsters revealed that the exposure of hamsters to the smoke of one cigarette elicits the rolling and adhesion of fluorescently labeled leukocytes to the endothelium of small venules and arterioles in striated muscle (11). Leukocyte adhesion was significantly reduced by pretreatment of the animals with superoxide dismutase, implying a key mediator role for superoxide radicals in CS-induced leu...

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“…It is thus possible that the emphysema observed in the current study may be related to their sensitivity to oxidants. Chronic oxidative stress may have resulted in emphysema either via a direct effect on lung matrix components and/or via indirect effects, such as inactivation of a 1 -PI [14], and/or sequestration of neutrophils in the lung microvasculature [15]. Both these two latter factors may have contributed to the increase in elastolytic burden.…”

Section: Discussionmentioning

confidence: 99%

Different lung responses to cigarette smoke in two strains of mice sensitive to oxidants

Bartalesi¹

2005

Eur Respir J

152

113

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The development of cigarette smoke-induced pulmonary changes in C57 Bl/6J and DBA/2 mice was investigated. Both strains are sensitive to oxidants and C57Bl/6J mice are moderately deficient in serum alpha1-proteinase inhibitor.Following chronic exposure to cigarette smoke, patchy emphysema was present in mice of both strains, but developed faster in DBA/2 mice. A positive reaction for mouse neutrophil elastase was seen on the septa of both strains. Additionally, the DBA/2 mice developed a uniform parenchymal dilation that was preceded by the appearance of apoptotic cells in areas with a low signal for vascular endothelial growth factor-receptor 2. Fibrotic areas scattered throughout the parenchyma, coupled with a positive immunohistochemical reaction for transforming growth factor-b was seen only in DBA/2 mice.Both DBA/2 and C57Bl/6J strains showed epithelial cell injury and areas of deciliation in their airways. However, the appearance of goblet cell metaplasia was common in C57Bl/6J mice but rare in DBA/2 mice. A positive immunohistochemical reaction for interleukin (IL)-4, IL-13 and MUC5AC was seen only in the airways of C57Bl/6J mice.Strain characteristics (alpha1-proteinase inhibitor levels, sensitivity to oxidants, and constitutive levels of vascular endothelial growth factor-receptor 2) and phenotypical responses (apoptosis and cytokine distribution) may condition parenchymal and airway changes to cigarette smoke.

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Decreased Leukocyte Deformability after Acute Cigarette Smoking in Humans

Cited by 46 publications

References 32 publications

Increased exhalation of hydrogen peroxide in healthy subjects following cigarette consumption

Increased exhalation of hydrogen peroxide in healthy subjects following cigarette consumption

Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo.

Different lung responses to cigarette smoke in two strains of mice sensitive to oxidants

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