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PubMed1993

Differences between smokers and never-smokers in sensitivity to nicotine: a preliminary report.

Sensitivity to nicotine was explored using test doses administered via intra-nasal aerosol in 10 smokers and 10 never-smokers. Smokers received 1.50 mg nicotine (in 2 sprays, < 5 seconds apart, one spray per nostril); never-smokers received either 0.50 mg (n = 3) or 0.25 mg (n = 7) nicotine. Accumulation of nicotine in plasma, per unit dose administered, was nearly four times greater in never-smokers than in smokers, indicating differences in pharmacokinetic tolerance. To examine sensitivity to nicotine without this confound, peak physiological reactivity (heart rate and blood pressure changes) was divided by peak plasma nicotine increment and the ratio was expressed as a function of cotinine level prior to dosing, thereby relating sensitivity to nicotine to history of exposure. In smokers, functional sensitivity to nicotine was inversely related to customary nicotine intake, replicating previous findings for light and heavy smokers. The observation that never-smokers were not much more sensitive to nicotine than light smokers is notable given the disparity in previous history of exposure.

Administration, Intranasal↗
PubMed1984

Toothbrushing efficiency in smokers and non-smokers.

The present study was conducted to determine whether smokers have more plaque than non-smokers, and whether higher plaque scores subsequently found in smokers could be explained by differences in toothbrushing time, efficiency and frequency. Plaque was scored from photographs, before and after toothbrushing, in 64 smokers and 64 non-smokers, aged 20-40 years, matched for age and sex. The results showed that in both sexes smokers had more plaque than non-smokers. Male smokers brushed for a shorter time, and had more plaque after toothbrushing, than male non-smokers. A similar, though non-significant trend was found in females. There was no association between tobacco consumption and frequency of toothbrushing. It was concluded that the poorer oral cleanliness found in smokers both before and after toothbrushing may be explained, in part at least, by their shorter toothbrushing time.

Adult↗
PubMed1990

Decline of lung function and development of chronic airflow limitation: a longitudinal study of non-smokers and smokers in Busselton, Western Australia.

Data collected during seven population health surveys over 18 years in Busselton, Western Australia, were examined to determine the effect of smoking on lung function and to investigate the development of chronic airflow limitation. Lung function was measured and details of respiratory illness and smoking histories were collected from subjects attending surveys at three year intervals from 1966 to 1984. Data from ex-smokers and asthmatic patients (diagnosis based on answer to questionnaire) were excluded. Regression of height adjusted forced expiratory volume in one second (FEV1) on age was calculated individually for 759 non-smokers and 225 regular smokers with four or more observations. Decline in height adjusted FEV1 was similar for men and women. In smokers the rate of decline in FEV1 was greater than in non-smokers and was related to the amount smoked, to the extent that a smoker could expect a 20-30% greater rate of decline than a non-smoker of the same age. Chronic airflow limitation (defined as FEV1/FEV less than 65% or FEV1 less than 65% predicted on at least two occasions) was common, occurring in 24% of men and 18% of women who were regular smokers and in 5% of male and 8% of female non-smokers. These figures are higher than those reported in other populations, especially for women and for non-smokers. Not all chronic airflow limitation was associated with respiratory symptoms, confirming that the condition may be unrecognised until it is advanced.

Adult↗
PubMed1986

Mean transit time, forced expiratory volume and age in healthy male smokers and non-smokers.

We studied 67 healthy males aged 20-30 years, 29 of them non-smokers and 38 smokers. In smokers, forced expiratory volume (FEV), 1 s forced expiratory volume (FEV1) and peak flow (PF) were significantly lower than in non-smokers, while the FEV1/FEV ratio, flows and mean transit time (MTT) compared well. MTT appeared directly related to age and negatively to FEV1/FEV, with no difference between the two groups, but MTT was directly related to FEV in non-smokers and negatively in smokers. Multiple regression analysis, MTT = a + b(FEV)+c(age), showed that parameters b and c were significantly different between smokers and non-smokers and, in the former, parameter b was negative. In non-smokers the effects of age and FEV on MTT were roughly the same, but in smokers MTT was influenced above all by age, probably because MTT measured the effects of continued smoking.

Adult↗
PubMed2000

Respiratory decline in smokers and ex-smokers--an independent risk factor for cardiovascular disease and death.

BACKGROUND AND OBJECTIVE: Although smoking is associated with an increased incidence of cardiovascular disease and death, many smokers remain healthy after many years of smoking. Our objective was to assess whether this variation is related to rate of decline of respiratory function. DESIGN: This was a population-based cohort study, its subjects being men born in 1914 from Malmö, Sweden. METHODS: All 291 smokers who since the baseline examination in 1969 had remained in Malmö were invited to a follow-up examination in 1982. Of the 242 participants, 199 men without history of myocardial infarction or stroke were included in the study. Eighty-four of them had quit smoking. The incidence of cardiovascular disease and death during 14 years was studied in relation to the decline in lung function [forced expiratory volume during 1 second (FEV1.0) and vital capacity] between 55 and 68 years of age. RESULTS: Fifty-nine (51%) smokers and 43 (51%) ex-smokers died. Forty-four (38%) smokers and 29 (35%) ex-smokers suffered a cardiovascular event. The mortality rate among smokers in the high, middle and low thirds with regard to the decline in FEV1.0 was 66.5, 44.0, and 37.6, respectively, per 1000 person-years (P for trend = 0.04). The corresponding figures in ex-smokers were 88.7, 42.0, and 35.1 (P for trend = 0.002). The cardiovascular event rate among smokers in these three groups was 56.0, 41.0, and 22.7 events, respectively, per 1000 person-years (P for trend = 0.01). The association remained significant after adjustments for potential confounders. A change in vital capacity was associated with a similar pattern of disease and death. CONCLUSION: Although smoking is associated with an accelerated respiratory decline, there are marked differences between smokers. The increased cardiovascular event and death rates among those whose lung function declined the most suggests that the change in respiratory function can be used as a measure of individual susceptibility.

Age Factors↗
PubMed1999

Calculation of risk for the development of acute myocardial infarction in the normal population based on long-term follow-up studies: smokers compared with non-smokers.

The objective was to study the association between smoking habits and mortality from coronary heart disease among men and women aged 35-49 years. Almost 45000 individuals (50% women) from three counties in Norway attended a screening programme during 1974-1978. The participation rate was almost 90% of the population. These individuals have been followed for an average of 18 years through the Norwegian death register. There were 1021 and 193 deaths from coronary heart disease among men and women, respectively. The mortality rate among current smokers was three times higher than that among those who had never smoked cigarettes. The relative risk between low-dose smokers and non-smokers was higher than that between high- and low-dose smokers. Among men, the relative risk between smokers and non-smokers was lower in the age group 45-49 years than in the two younger 5-year age groups. Among women, the relative risks did not vary significantly across the age groups. The relative risk between smokers and non-smokers remained the same in the first and second half of the observation period in men. A stronger association in the second half of the observation period was suggested among women (P = 0.08). The duration of smoking was an independent predictor of coronary heart disease among men, but not among women. Duration of smoking and length of follow-up seemed to have a different relationship with mortality from coronary heart disease in men and women. The dose-response relationship was the same in men and women, on the relative scale. Age affected the magnitude of relative risk between smokers and non-smokers among men, but not among women.

Adult↗
PubMed2006

The detection of salivary minerals in smokers and non-smokers with chronic periodontitis by the inductively coupled plasma-atomic emission spectrophotometry technique.

BACKGROUND: The purpose of this study was to evaluate the effect of smoking on the salivary minerals in subjects with chronic periodontitis by the inductively coupled plasma-atomic emission spectrophotometry (ICP-AES) technique. METHODS: The study group included 24 subjects-12 smokers and 12 non-smokers-with chronic periodontitis. Clinical measurements and non-stimulated whole saliva were obtained, and the levels of five elements-sodium, potassium, calcium, magnesium, and phosphate-in each specimen were analyzed. RESULTS: When the clinical parameters were compared between groups, only plaque index was significantly higher in smokers than non-smokers (P <0.05). The mean plaque index of smokers and non-smokers was 1.93 +/- 0.51 and 1.51 +/- 0.39, respectively. The results of this study showed that there were no significant differences between groups in the mineral content of saliva. In smokers, there were positive correlations between the levels of calcium, sodium, and magnesium and clinical attachment level. There was also a positive correlation between the level of phosphate and the percentage of bleeding on probing. In non-smokers, there was a negative correlation only between the mean level of sodium and plaque index (P <0.05). CONCLUSIONS: The present study showed that no significant differences were found between the mineral content of saliva of smokers and non-smokers by the ICP-AES technique. It is a useful, fast, and sensitive technique compared to other techniques, and it can be advised for researchers while analyzing the mineral content of saliva.

Adult↗
PubMed2006

Periodontal status in smokers and never-smokers: clinical findings and real-time polymerase chain reaction quantification of putative periodontal pathogens.

BACKGROUND: Smoking is a well-known risk factor for destructive periodontal disease, but its relationship with periodontal status and subgingival microbiota remains unclear. Inherent limitations of microbiological methods previously used may partly explain these mixed results, and real-time polymerase chain reaction (PCR) has been presented as a valid alternative. The aim of the present study was to investigate the clinical condition and microbiological profile of patients with chronic periodontitis as related to the habit of smoking. METHODS: Fifty patients (33 to 59 years old), 25 smokers and 25 never-smokers, constituted the sample. The visible plaque index (VPI), gingival bleeding index (GBI), bleeding on probing (BOP), periodontal probing depth (PD), clinical attachment loss (CAL), and gingival crevicular fluid (GCF) volume were recorded. Real-time PCR quantified Porphyromonas gingivalis, Micromonas micros, Dialister pneumosintes, Actinobacillus actinomycetemcomitans and total bacteria in subgingival samples. RESULTS: Smokers and never-smokers showed similar values for VPI, GBI, and BOP. Smokers had deeper PD in buccal/lingual sites and higher CAL independently of the tooth surface. The GCF volume was smaller in smokers, independent of the PD. Similar amounts of total bacteria and P. gingivalis were observed for both groups. Significantly higher numbers of D. pneumosintes and M. micros were present in smokers and associated with moderate and deep pockets. When heavy smokers were considered, higher counts of total bacteria, M. micros, and D. pneumosintes were observed. CONCLUSIONS: Smoking seems to have a detrimental impact on the periodontal status and microbiological profile of patients with periodontitis. Compared to never-smokers, smokers had deeper pockets, greater periodontal destruction, and higher counts of some putative periodontal pathogens.

Adult↗
PubMed2007

Gingival crevicular fluid prostaglandin E(2) and thiobarbituric acid reactive substance levels in smokers and non-smokers with chronic periodontitis following phase I periodontal therapy and adjunctive use of flurbiprofen.

BACKGROUND: It has been established that smoking is an important risk factor for the initiation and progression of chronic periodontitis (CP). This study investigates the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on prostaglandin E(2) (PGE(2)) and thiobarbituric acid reactive substance (TBARS) levels in gingival crevicular fluid (GCF) samples from smoker and non-smoker patients with CP. METHODS: Twenty-one non-smoker and 21 smoker patients with CP were divided into four groups according to treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 x 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 x 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded and GCF samples were collected at baseline and on day 10 of drug intake from each sampling area by a single examiner who was unaware of the treatment modality. Assays for GCF PGE(2) and TBARS were carried out by an enzyme-linked immunosorbent assay and fluorometric method, respectively. RESULTS: All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment on day 10 (P <0.05), but no statistical differences were observed in PD and CAL scores after the therapy. In groups 1 and 2, the reduction of GCF PGE(2) and TBARS levels were not significant after the therapy compared to baseline levels. In group 3, GCF PGE(2) and TBARS levels exhibited a statistically significant decrease (P <0.05) after the therapy. Group 4 showed significant reductions (P <0.05) in GCF PGE(2) levels after the therapy. No statistically significant reductions were observed in group 4 with regard to GCF TBARS levels. When groups 1 and 3 were compared according to GCF TBARS levels after the therapy, a more statistically significant reduction was observed in group 3 (P = 0.001). CONCLUSION: These results suggest that additional flurbiprofen administration may have more inhibitory effects on GCF levels of PGE(2) and TBARS in the groups of smokers compared to non-smokers with CP.

Adult↗
PubMed2005

Dental death rate prevalence in smokers and non smokers adults with periodontal disease.

The current study target was to evaluate the dental loss pattern in an adult population with periodontal disease who was treated at the Periodontal Chair, Dentistry Faculty, National University of Rosario, Argentina. The sample was of 203 patients, 130 women and 73 men; 75 of them were blond cigarette smokers and 128 of them were not in that habit. Inclusion criteria as follows: good systemic condition given by the absence of illnesses that may be risky for the development of a periodontal disease, and the presence of at least one teeth with insertion loss of 2 mm. minimum in its proximal faces. The age average of the group was 37,83 years (IC 95% 34,46-41,19) for smokers, and 40,98 (IC 95% 38,27- 43,69) years for non smokers. Regarding females, 85 of them were non smokers and 45 had that habit; concerning men 43 were non smokers and 30 were indeed. The independence test made under smoking and sex variables showed no significant relation between them. Regarding smoker group the smoked cigarette average per day (daily doses) was 13,27 cigarettes (IC 95% 10,96-15,57) and the time since habit started in measure of months was 193,57 (IC 95% 160,43-226,81). The death rate for tooth loss in each group was 4,71 teeth (CI 95 % 3,43-5,98) for smokers and 5,05 teeth (CI 95% 4,07-6,03) for non-smokers. Setting the probability of error of type I equal to 0.05, this study demonstrated that in this group of patients with periodontal disease, the tooth loss in smoker individuals was similar to the tooth loss in non-smoker individuals.

Adolescent↗
PubMed1990

[Pulmonary complications after thoracic surgery in smokers and non-smokers. A prospective study of 55 cases].

A prospective study was carried out between 1987 and 1989 at the Pneumological Department of the IRCCS-Policlinico S. Matteo in Pavia (Italy) to evaluate the incidence of postoperative pulmonary complications in smokers and non-smokers undergoing thoracic surgery for various diseases. Non-smokers were defined as those who had never smoked tobacco, while ex-smokers who had given up for over years were included in the "low consumption" group (less than 10 cigarettes/day). Out of a total of 55 cases, 75% were smokers. Complications developed in 20/55 cases (36.4%), whereas they were observed in 60% of the smokers' group. Major atelectasis developed in 8/20 (40%): 5 smokers and 3 non-smokers. Pulmonary complications were significantly higher among heavy smokers (greater than 10 cigarettes/day) than among non-smokers (p less than 0.001). The incidence of pulmonary complications in this study was thought to be satisfactory, although it could probably be further improved, given that daily postoperative chest X-rays and physical and/or pharmacological pre- and postoperative prophylaxis--in addition to continuous clinical monitoring--were performed. This strategy enabled complications to be detected early and controlled.

Aged↗
PubMed1985

Mucociliary clearance and airways obstruction in smokers, ex-smokers and normal subjects who never smoked.

On 17 ex-smokers (7 without chronic bronchitis, 10 with chronic bronchitis) and 48 smokers (13 without chronic bronchitis, 35 with chronic bronchitis) we analyzed the correlation between smoking habits (pack years, smoking and ex-smoking time), mucociliary clearance rate (mC) and airways obstruction. The mC was measured with 99mTc tagged monodisperse erythrocytes. The static and dynamic lung volumes, the maximal expiratory flow volume curve and the airway resistance were measured by whole body plethysmography. The ex-smokers without chronic bronchitis showed the same mucociliary clearance rate (t-mC in 1 h = 38.3 +/- 10.3%) as the 80 control subjects who never smoked (t-mC in 1 h = 36.9 +/- 12.6%). But the subjects who never smoked showed less airway obstruction. The mucociliary clearance rate in normal subjects who never smoked is a function of age: t-mC in 1 h = -0.37 X age + 53; c-mC in 1 h = -0.45 X age + 73; p-mC in 1 h = -0.25 X age + 38. The smokers without chronic bronchitis showed normal ventilatory function tests but a lower mC rate (t-mC in 1 h = 27.8 +/- 12.3%) than the healthy ex-smokers and the control subjects who never smoked (p less than 0.01). The ex-smokers and smokers with chronic bronchitis had a lower mC rate (t-mC in 1 h = 21.2 +/- 11.3% and 18.1 +/- 9.1) and more airway obstruction (p less than 0.001) than the subjects who did not report any symptoms of chronic bronchitis. The ex-smokers with persistent symptoms of chronic bronchitis showed the severest degree of airways obstruction. The smokers with chronic bronchitis showed the most delayed central mC (c-mC) rate, but less airway obstruction than the ex-smokers with persistent symptoms of chronic bronchitis. The smoking habits (pack years) correlated with the decreased mC rate (p less than 0.01) and the degree of airways obstruction (p less than 0.001).

Adult↗
PubMed2005

Multiplicity of abnormal promoter methylation in lung adenocarcinomas from smokers and never smokers.

The prevalence of methylation of the p16, DAPK and RASSF1A genes was investigated in lung adenocarcinoma from smokers, former uranium miners and never smokers. The association between a common genetic alteration in adenocarcinoma, mutation of the K-ras gene and methylation of these genes, as well as survival was examined. Adenocarcinomas from 157 smokers, 46 never smokers and 34 former uranium miners were evaluated for methylation of the p16, DAPK and RASSF1A genes using the methylation-specific PCR assay. Comparisons were also made to prevalences of methylation of the MGMT gene and mutation of the K-ras gene previously examined in these tumors. The prevalence of methylation for all genes was similar between adenocarcinomas from smokers and never smokers, although the prevalence for methylation of the p16 gene tended to be higher in smokers compared to never smokers. A significantly higher prevalence for p16 methylation was seen in central vs. peripheral lung tumors. At least 1 gene was methylated in 35% of stage I tumors, whereas 2 and >/=3 genes were methylated in 40% and 16% of tumors, respectively. Methylation of all genes was independent of K-ras mutation, whereas methylation of the DAPK and RASSF1A genes was positively associated. Environmental tobacco smoke, the strongest lung cancer risk factor among never smokers, induces adenocarcinoma in part through inactivation of the p16, DAPK and RASSF1A genes. Adenocarcinomas may develop through 2 distinct processes: multiple gene inactivations through promoter hypermethylation and activation of the K-ras gene.

Adenocarcinoma↗
PubMed1993

Alkylation and oxidative-DNA damage repair activity in blood leukocytes of smokers and non-smokers.

The levels of 3 DNA repair enzymes involved in alkylation and oxidative DNA damage repair in human peripheral blood leukocytes were measured in 20 smokers and 17 non-smokers. No differences in O6-alkylguanine-DNA-alkyltransferase (AGT) activity were found between the 2 groups and the AGT distribution within the population appeared to be unimodal. In contrast, the mean activities of both the methylpurine (MeP)- and the 2-6-diamino-4-hydroxy-5N formamidopyrimidine (FaPy)-DNA glycosylases were higher in the smokers, although only the difference between the MeP-DNA glycosylase means was statistically significant. The standard deviations of these 2 enzymes were also higher in the smokers. The MeP-DNA glycosylase activity showed a bimodal distribution when all subjects were considered. This may in part be due to the smoking habit; 83% of the subjects with enzyme activities higher than 500 fmoles/mg protein were current smokers, whilst 85% of the non-smokers had lower enzyme activities. However, if the smokers were considered separately, a bimodal distribution of this enzyme activity could still be observed. No strong correlation was observed between enzyme activity and age, although the slopes of the regression lines of enzyme activity on age were all negative. The relationship between enzyme activities was studied by bivariate distribution and a strong correlation was only found between the MeP-DNA glycosylase and the FaPy-glycosylase, with the highest values of both enzyme activities being observed in the smokers and the lowest in the non-smokers. Our results suggest that the activity of certain DNA repair enzymes can be modulated by environmental exposure.

Adult↗
PubMed1989

Levels of benzene and other volatile aromatic compounds in the blood of non-smokers and smokers.

The concentrations of benzene, toluene, ethylbenzene, and o-, m-and p-xylene were measured in venous blood samples collected from 13 non-smokers and 14 cigarette smokers. The blood samples were analysed by a purge and trap technique followed by gas chromatography/mass spectrometry/computer analysis. The above-mentioned volatile organic compounds (VOC) could be detected in measurable amounts in all blood samples. This finding seems to reflect the ubiquitous exposure of humans to these agents in the urban environment, in non-smokers as well as in smokers. Smokers were found to have significantly higher blood concentrations of benzene (median 547 ng/l) and toluene (median 2201 ng/l) than non-smokers (median 190 ng/l and 1141 ng/l, respectively). The concentrations of ethylbenzene and xylenes also tended to be higher in smokers when compared to non-smokers. The different concentrations of these compounds in the blood of non-smokers appear to reflect the common concentration pattern found in outdoor urban air as well as in indoor air and also seem to be influenced by the different blood/air partition coefficients of these compounds. The results indicate that smoking is associated with a significant additional exposure to VOC, in particular to benzene and toluene.

Benzene Derivatives↗
PubMed2005

The influence of vitamin C on systemic markers of endothelial and inflammatory cell activation in smokers and non-smokers.

OBJECTIVE AND DESIGN: To determine the influence of vitamin C supplementation (500 mg, bd, 14 days) on the circulating concentrations of soluble ICAM-1 (a marker of endothelial activation), neopterin (a marker of monocyte activation), and neutrophil elastase (a marker of neutrophil activation) in smokers and non-smokers in a randomised, double-blind, placebo-controlled trial in a hospital setting. SUBJECTS: Twenty smokers (serum cotinine > or = 20 ng ml(-1)) and 20 age- and gender-matched non-smokers (serum cotinine < or = 13.7 ng ml(-1)). RESULTS: At baseline, there was a significant elevation in the concentration of sICAM-1 in smokers (median 247, IQR 199 to 357 ng ml(-1)) compared to non-smokers (median 207, IQR 189 to 227 ng ml(-1); p = 0.014). Vitamin C supplementation did not influence the circulating concentrations of ICAM-1 or neopterin, or leukocyte elastase activity, in smokers, non-smokers, or in the total population. CONCLUSIONS: Markers of monocyte and neutrophil activation were not influenced by smoking status in this study population. However, sICAM-1 concentrations were significantly elevated in tobacco smokers, reflecting tobacco-induced vascular activation that is unaffected by Vitamin C supplementation.

Adult↗
PubMed1985

Differential enhancement of sister-chromatid exchange frequencies by alpha-naphthoflavone in cultured lymphocytes from smokers and non-smokers.

The sister-chromatid exchange (SCE) frequency was assessed in peripheral lymphocytes from 4 smokers and 8 non-smokers in the absence or presence of alpha-naphthoflavone (ANF) in the culture media. ANF produced a concentration-dependent increase in the frequency of SCEs in smoking individuals. At an ANF concentration of 11 micrograms/ml, average SCE levels were 54% and 13% above the baseline levels in smokers and non-smokers, respectively. The ANF-enhanced increase in the SCE frequency ranged from 3.12 to 5.72 among smokers, and from 0 to 1.96 among the non-smokers. No significant difference in the mean SCE baseline levels between smokers and non-smokers was detected. The mechanism responsible for the enhanced frequency of SCEs in smokers following in vitro exposure to ANF is not clear, but may reflect changes in metabolic activation/deactivation or increased sensitivity to genetic effects of ANF.

Adult↗
PubMed2006

Macrophage-stimulating protein differently affects human alveolar macrophages from smoker and non-smoker patients: evaluation of respiratory burst, cytokine release and NF-kappaB pathway.

Macrophage activation is a key feature of inflammatory reactions occurring during bacterial infections, immune responses and tissue injury. We previously demonstrated that human macrophages of different origin express the tyrosine kinase receptor recepteur d'origine nantaise, the human receptor for MSP (RON) and produce superoxide anion (O(2)(-)) when challenged with macrophage-stimulating protein (MSP), the endogenous ligand for RON. This study was aimed to evaluate the role of MSP in alveolar macrophages (AM) isolated from healthy volunteers and patients with interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis), either smokers or non-smokers, by evaluating the respiratory burst, cytokine release and nuclear factor-kappa B (NF-kappaB) activation. MSP effects were compared with those induced by known AM stimuli, for example, phorbol myristate acetate, N-formyl-methionyl-leucyl-phenylalanine, lipopolysaccharide.MSP evokes O(2)(-) production, cytokine release and NF-kappaB activation in a concentration-dependent manner. By evaluating the respiratory burst, we demonstrate a significantly increased O(2)(-) production in AM from healthy smokers or smokers with pulmonary fibrosis, as compared to non-smokers, thus suggesting MSP as an enhancer of cigarette smoke toxicity. Besides inducing interleukin-1 beta (IL-1beta) and interleukin-10 (IL-10) production, MSP triggers an enhanced tumor necrosis factor-alpha release, especially in healthy and pulmonary fibrosis smokers. On the contrary, MSP-induced IL-10 release is higher in AM from healthy non-smokers. MSP activates the transcription factor NF-kappaB; this effect is more potent in healthy and fibrosis smokers (2.5-fold increase in p50 subunit translocation). This effect is receptor-mediated, as it is prevented by a monoclonal anti-human MSP antibody. The higher effectiveness of MSP in AM from healthy smokers and patients with pulmonary fibrosis is suggestive of its role in these clinical conditions.

Aged↗