Tobacco Smoke Induces Coordinate Activation of HSF and Inhibition of NFκB in Human Monocytes: Effects on TNFα Release

Vayssier, Muriel; Favatier, Florence; Pinot, Françoise; Bachelet, Maria; Polla, Barbara S.

doi:10.1006/bbrc.1998.9586

Cited by 56 publications

(30 citation statements)

References 30 publications

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“…To date, several reports have found NF-B inhibitory effects of tobacco smoke or tobacco smoke components (43)(44)(45)(46)(47), but the underlying mechanisms remained unclear. In our study, examination of the NF-B activation pathway showed that ETS decreased the levels of phosphorylated IKK␣/␤, suggesting inhibition of these kinases.…”

Section: Discussionmentioning

confidence: 99%

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Zhong

Zhou

Joad

et al. 2006

Am J Respir Crit Care Med

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Rationale: Exposure to environmental tobacco smoke in early life has adverse effects on lung development. Apoptosis plays an essential role in development; however, the molecular mechanisms of pulmonary apoptosis induced by environmental tobacco smoke is unknown. Objectives: To investigate the mechanistic role of nuclear factor (NF)-B, a critical cell survival pathway, in the developing lungs exposed to environmental tobacco smoke.

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Section: Discussionmentioning

confidence: 99%

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Zhong

Zhou

Joad

et al. 2006

Am J Respir Crit Care Med

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“…35 There are several possible pathways linking inhaled tobacco smoke, which is reflected by the amount of COHb%, to atherosclerosis. The toxicity of inhaled tobacco could by caused by a variety of compounds including reactive oxygen species, eg, causing DNA damage, 36 inhibition of the transcription nuclear factor kappa B (NFB) in human monocytes 37 and production of platelet activator factor, 38 nitric oxide modified substances, 39 glycotoxines, 40 endotoxins, 41 and substances stimulating the production of isoeicosanoids. 42 Smokers with reduced lung function comprise another group at risk for cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Lind

Engström

Stavenow

et al. 2004

ATVB

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Background-The extent to which differences in cardiovascular risk between smokers with similar daily tobacco consumption may be related to plasma levels of inflammation-sensitive proteins (ISP) and whether these proteins are associated with levels of carboxyhemoglobin (COHb%) have not been clarified. Methods and Results-In a population-based cohort of 1489 never smokers, 1685 former smokers, and 2901 current smokers, aged 28 to 61 years, plasma levels of orosomucoid (␣ 1 -acid glycoprotein), ␣ 1 -antitrypsin, haptoglobin, fibrinogen, and ceruloplasmin were measured. COHb% levels were available for 2098 of them. Incidence of myocardial infarction, stroke, and death were monitored over 18.7Ϯ4.7 years. The proportion with high ISP levels (ie, Ն2 ISP in the top quartile) increased progressively with daily tobacco consumption (PϽ0.01) and COHb% (PϽ0.01). In all smoking categories, the incidence of stroke, cardiac events, and death was related to ISP. In heavy smokers, high ISP levels were associated with adjusted relative risks of 1.57 (1.05 to 2.35) and 1.50 (1.11 to 2.03) for cardiac events and death, respectively. Corresponding figures for moderate and light smokers were 1.59 (1.13 to 2.24) and 1.14 (0.87 to 1.49), respectively, and 1.32 (0.95 to 1.85) and 1.48 (1.10 to 1.98), respectively. Key Words: stroke Ⅲ myocardial infarction Ⅲ smoking Ⅲ inflammation Ⅲ plasma proteins Ⅲ epidemiology S moking is one of the major risk factors for arteriosclerosis and its complications. [1][2][3] Yet how smoking harms the vessel wall remains controversial. The biological mechanism linking smoking and atherothrombosis is complex and not fully understood 4 and include vascular endothelial dysfunction, 5 systemic coagulation disturbances, 6 and lipid disorders. 7 It has been demonstrated in several cohort studies that the incidence of myocardial infarction and stroke are associated with plasma level of interleukin-6 (IL-6), 8 tumor necrosis factor-␣ (TNF-␣), 9 soluble intracellular adhesion molecule type 1 (ICAM-1), 10 E-selectin, 11 P-selectin, 12 high sensitive C-reactive protein (CRP), 13,14 and other inflammatory-sensitive proteins (ISP), eg, fibrinogen, orosomucoid (␣ 1 -acid glycoprotein), ␣ 1 -antitrypsin, haptoglobin, and ceruloplasmin. 15,16 Plasma levels of inflammatory markers are generally higher in smokers compared with nonsmokers. 17,18 Between smokers with equal tobacco consumption there are, however, great variations of the cardiovascular risk. This may be related to the amount of harmful components in the tobacco smoke that is absorbed into the blood. Carboxyhemoglobin (COHb%), which in prospective studies has been identified as a predictor of cardiovascular disease in smokers, 19 may vary substantially within categories defined in terms of daily consumption. Whether and how the cardiovascular risk in smokers is related to the plasma levels of ISP and whether the amount of these proteins has any relationship with the level of COHb% is largely unknown. 20 The objectives in this prospective cohort study have been to...

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“…22 Moreover, in other studies, nicotine was observed to significantly decrease the secretion of inflammatory mediators in human monocyte-macrophages by inhibiting activation of nuclear factor (NF)-κB. 32,33 It has been suggested that nicotine could be an important regulator of monocytemacrophages, through its role in the cholinergic antiinflammatory pathway, [34][35][36] mediated, in part, by inhibiting NF-κB and activating the transcription factor STAT3, a negative regulator of inflammation, via interaction with acetylcholine receptor α-7. 37 Contrary to the evidence showing antiinflammatory properties of smoking in monocytemacrophages, most 38,39 but not all studies 40 have reported a negative correlation between cigarette smoking and adiponectinemia, a well-known antiinflammatory adipokine that increases PPARG and insulin sensitivity.…”

Section: Circulation Journal Vol73 November 2009mentioning

confidence: 93%

Pro12Ala Polymorphism of the Peroxisome ProliferatorActivated Receptor-.GAMMA. Gene is Associated With Metabolic Syndrome and Surrogate Measures of Insulin Resistance in Healthy Men Interaction With Smoking Status

Tellechea

Aranguren

Pérez

et al. 2009

Circ J

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Background:The Pro12Ala polymorphism (rs1801282), a nonsynonymous substitution of peroxisome proliferator-activated receptor-γ (PPARG), has been robustly associated with type 2 diabetes. However, its role in metabolic syndrome (MetS) remains poorly understood. The associations among rs1801282, MetS and surrogate measures of insulin resistance (IR) were investigated in the present study. Methods and Results:A cross-sectional population-based survey of 572 unrelated healthy male Argentinian blood donors with normal findings on medical examination and not taking any medication was conducted. MetS was assessed using the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III) criteria, and the HOMA-IR, and QUICKI were calculated. Genotyping of rs1801282 was performed using RFLP-PCR. The prevalence of MetS was 26.2%. The Pro/Ala genotype (and the Ala12 allele) was associated with a high risk for MetS (odds ratio (OR) 1.67 [95% confidence interval (CI) 1.03-2.72], P=0.0394). This was highlighted among nonsmokers (OR 2.20 [95%CI 1.25-3.88], P=0.0059). ANCOVA confirmed an interaction between smoking status and this association (P=0.031). Ala12 carriers had a higher waist circumference than noncarriers (P=0.0065). Among nonsmokers, surrogates of IR, such as HOMA-IR, were significantly higher in Ala12 carriers than in noncarriers (P<0.05). Conclusions: Healthy men, in particular nonsmokers, carrying the Ala12 allele of PPARG rs1801282 polymorphism, have a high risk for MetS and IR. (Circ J 2009; 73: 2118 -2124

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Tobacco Smoke Induces Coordinate Activation of HSF and Inhibition of NFκB in Human Monocytes: Effects on TNFα Release

Cited by 56 publications

References 30 publications

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Pro12Ala Polymorphism of the Peroxisome ProliferatorActivated Receptor-.GAMMA. Gene is Associated With Metabolic Syndrome and Surrogate Measures of Insulin Resistance in Healthy Men Interaction With Smoking Status

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