Bronchial Reactivity, Lung Function, and Serum Immunoglobulin E in Smoking-discordant Monozygotic Twins

Ericsson, Carl Henrik; Svartengren, Magnus; Mossberg, B; Camner, Per

doi:10.1164/ajrccm/147.2.296

Cited by 21 publications

(12 citation statements)

References 27 publications

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“…In addition, one study excludes genetic factors by assessing IgE levels in monozygotic twin pairs who are discordant for smoking. It was found, as in other studies, that smokers have elevated serum IgE levels (Ericsson et al, 1993). Even ex-smokers have higher IgE levels than never-smokers; however, unlike the situation in current smokers, IgE levels in this group decrease with age (Shirakawa et al, 1992).…”

Section: Effects Of Tobacco and Smoking On Ige Levelssupporting

confidence: 68%

“…However, at least one study indicates that PHAinduced IL-4 production is elevated in T-cells from smokers (Byron et al, 1994). This elevation is consistent with the increased levels of serum IgE and incidences of atopy that are associated with cigarette smoking (O'Connor et al, 1989;Criqui et al, 1990;Bonnin et al, 1991;Jensen et al, 1992;Ericsson et al, 1993). In addition, there are reports that IL-2 production is elevated in splenic T-cells isolated from rats infused with nicotine (Petro et al, 1992).…”

Section: Effects Of Smoking and Tobacco On T-lymphocyte Cytokine Prodmentioning

confidence: 72%

“…Many investigators have observed that adult serum levels of IgE are elevated in smokers compared with nonsmokers (O'Connor et al, 1989;Criqui et al, 1990;Bonnin et al, 1991;Jensen et al, 1992;Ericsson et al, 1993). This effect seems to be more common in males than in females (Barbee et al, 1987;Criqui et al, 1990;Bonnin et al, 1991;Jensen et al, 1992;Shirakawa et al, 1992), and there is a dose-response relationship in the sense that increased pack-years correlate with increased IgE levels (Criqui et al, 1990;Jensen et al, 1992;Shirakawa et al, 1992;Sherrill et al, 1994).…”

Section: Effects Of Tobacco and Smoking On Ige Levelsmentioning

confidence: 99%

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Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Barbour

Nakashima

Zhang

et al. 1997

Critical Reviews in Oral Biology & Medicine

233

182

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This review summarizes the current data on the effects of smoking and tobacco on the immune system and its potential impact on periodontal health. Smokers are 2.5-6 times more likely to develop periodontal disease than non-smokers, and there is evidence for a direct correlation between the number of cigarettes smoked and the risk of developing disease. Tobacco users also tend to exhibit increased severity of periodontal disease. Direct correlations between tobacco use and increased attachment loss and pocket depth and reduced bone crest height have been reported. Although the correlation between tobacco use and periodontal disease is quite strong, the role of tobacco in the pathogenesis of periodontal disease is uncertain. Recent studies indicate that one potential mechanism is that tobacco use exacerbates periodontal disease because it alters the immune response to periodontal pathogens. Indeed, smokers exhibit increased numbers of peripheral blood mononuclear phagocytes which appear to be functionally compromised. Inadequate phagocyte activity could reduce the clearance of pathogens from the oral cavity and thereby facilitate the development of periodontal disease. Tobacco-exposed B- and T-lymphocytes exhibit reduced proliferative capacities which could limit the production of protective immunoglobulins against oral pathogens. The risk factors for periodontal disease can be broadly classified as genetic, environmental, host-response factors, and host-related factors such as age. Tobacco, an environmental factor, undermines the host response and may facilitate the development and progression of periodontal disease. This review highlights the inter-relatedness of two of the risk factors associated with periodontal disease.

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Section: Effects Of Tobacco and Smoking On Ige Levelssupporting

confidence: 68%

Section: Effects Of Smoking and Tobacco On T-lymphocyte Cytokine Prodmentioning

confidence: 72%

Section: Effects Of Tobacco and Smoking On Ige Levelsmentioning

confidence: 99%

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Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Barbour

Nakashima

Zhang

et al. 1997

Critical Reviews in Oral Biology & Medicine

233

182

View full text Add to dashboard Cite

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“…Since the effect of IL-8 as a chemotactic factor is mainly on neutrophils, the increase in eosinophils in BL may simply be seen as a side-effect phenomenon. Alternatively, given the increase in capillary leakage due to airway inflammation, allergens may have easier access through the airways and this can elicit an "allergic" response with recruitment of eosinophils, as the increase of circulating IgE in smokers might suggest [28,29]. Another possibility is that, in the present study, the patient selection, although it was made using the internationally accepted criteria, may include some patients with an intrinsic asthmatic background relevant to the airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease

Pesci¹,

Balbi²,

Majori³

et al. 1998

Eur Respir J

285

190

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Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD) [1][2][3]. The pathogenesis of smoke-induced COPD has been evaluated in a number of studies showing the accumulation of inflammatory cells in patients' airways: predominantly polymorphonuclear leukocytes in samples representative of intraluminal infla-mmation (sputum, bronchial and bronchoalveolar lavage) and mainly mononuclear cells, lymphocytes and macrophages, in tissue specimens [4][5][6][7][8][9][10][11][12][13].While the reason (or reasons) for this discrepancy is still not completely clear, these studies have opened the field to new questions. Since the relevance of airway inflammation in COPD has been demonstrated, the next step is the characterization of the different features of airway inflammation, such as the nature of chemotactic signal(s) and the contribution of the various cell types to airway inflammation through the release of inflammatory mediators.In this regard, this study was targeted on a COPD patient population of nonatopic current smokers with airway obstruction, with the aim of investigating the characteristics of intraluminal airway inflammation in these patients. Therefore, this study evaluated the presence in bronchial lavage (BL) of: interleukin (IL)-8, a chemotactic factor for polymorphonuclear cells into the airways; myeloperoxidase (MPO), eosinophil cationic protein (ECP) and tryptase, mediators of tissue damage from polymorphonuclear cells and mast cells; and the correlations between cellular and noncellular data obtained from BL. Materials and methods Study subjectsTwelve patients with COPD entered this study. They all had chronic productive cough for >3 months for 2 consecutive yrs, in the absence of other known disorders, such as bronchiectasis, tuberculosis or lung cancer [14,15]. The patients met the following inclusion criteria: 1) history of cigarette smoking, with a minimum of 15 pack-yrs, in patients who all were current smokers at time of evaluation; 2) no occupational or other exposure to other substances known to cause lung disorders; 3) absence of atopy, i.e. with negative skin tests for common allergen These data suggest that cigarette smoke is associated with increased amounts of airway interleukin-8, a chemotactic factor for neutrophils and eosinophils. Recruited neutrophils and eosinophils are activated and they release increased amounts of inflammatory mediators capable of damaging the bronchial tissue. Eur Respir J 1998; 12: 380-386

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“…Recent Findings in smoking-discordant monozygotic twins that BHR does not seem to be a major risk factor for the development of early airways obstruction in smokers further support this conclusion [17], 202 Siekmeier/Buhl/Schultze-Werninghaus/ Kronenberger…”

Section: Discussionmentioning

confidence: 95%

Unspecific Bronchial Reactivity to Carbachol in Healthy Subjects – Effect of Age and Smoking Habits

Siekmeier

Buhl²,

Schultze‐Werninghaus³

et al. 1994

Respiration

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Chronic inflammatory processes of the airways induced by long-time cigarette consumption are a crucial factor in the pathogenesis of chronic obstructive pulmonary disease. In contrast, the role of cigarette smoking in the pathogenesis of bronchial hyperreactivity (BHR) is still unclear. The aim of this study was to assess the effect of chronic cigarette consumption on pulmonary function tests and BHR in healthy subjects. 63 healthy smokers and 63 lifetime nonsmokers matched for sex, age, height and weight were evaluated. Pulmonary function was determined by body plethysmography and spirometry. Bronchial provocation was performed by inhalation of increasing doses of carbachol (up to 25 g/l) in isotonic NaCl solution. Pulmonary function tests were within normal limits in all subjects. Nevertheless, midexpiratory flow at 25% of forced vital capacity was significantly smaller, and functional residual capacity was significantly greater in middle-aged smokers (age: 40-60 years) compared to middle-aged nonsmokers (p < 0.05, both comparisons). In young smokers and nonsmokers (age: 20-30 years) pulmonary function tests were not different (p > 0.28, all comparisons). Importantly, the carbachol concentration that provoked a 50% rise in specific airway resistance (PD₅₀sRaw) was similar in smokers and nonsmokers of both age groups (p > 0.05, both comparisons) and did not correlate with the age of the subjects (p > 0.2). No correlations between baseline values of pulmonary function tests and PD₅₀sRaw were observed (p > 0.34, all comparisons). The observations confirm that the distribution profile of BHR is unimodal and apparently not affected by age and smoking habits. Cigarette smoking likely has not a determining influence on the development of BHR.

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Bronchial Reactivity, Lung Function, and Serum Immunoglobulin E in Smoking-discordant Monozygotic Twins

Cited by 21 publications

References 27 publications

Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Tobacco and Smoking: Environmental Factors That Modify the Host Response (Immune System) and Have an Impact On Periodontal Health

Inflammatory cells and mediators in bronchial lavage of patients with chronic obstructive pulmonary disease

Unspecific Bronchial Reactivity to Carbachol in Healthy Subjects – Effect of Age and Smoking Habits

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