Tobacco smoking increases dramatically air concentrations of endotoxin

Larsson, Lennart; Szponar, Bogumiła; Pehrson, Christina

doi:10.1111/j.1600-0668.2004.00290.x

Cited by 92 publications

(83 citation statements)

References 9 publications

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“…Repeated exposure to endotoxin induces adaptation to further exposures by downregulating the inflammatory response [14]. Smokers are, like farmers, continuously exposed to organic compounds which also include endotoxin [15]. To our knowledge, there is no data regarding whether smokers, as a consequence of repeated exposure to tobacco smoke, develop adaptation to further exposure to tobacco smoke or other organic material.…”

mentioning

confidence: 86%

“…Cigarette smoke contains high levels of endotoxin and it has been demonstrated that smoking one cigarette results in the inhalation of 17.4 pmol of endotoxin and that indoor exposure to environmental tobacco smoke leads to the inhalation of 12.1 pmol of LPS?m -3 [15]. LAAN et al [36] showed that cigarette smoke extract inhibited LPS-induced production and mRNA expression of granulocyte macrophage colony-stimulating response in the most heavy smokers.…”

Section: Occupational and Environmental Lung Diseasementioning

confidence: 99%

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Repeated exposure to organic material alters inflammatory and physiological airway responses

Sundblad¹,

Schéele²,

Palmberg³

et al. 2009

European Respiratory Journal

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Farmers and smokers are repeatedly exposed to airborne organic material. We hypothesised that farmers and smokers show altered airway responses to inhaled organic, proinflammatory agents.A total of 11 farmers, 12 smokers and 12 controls underwent lipopolysaccharide (LPS) bronchial challenge and spent 3 h in a pig barn. Lung function, exhaled nitric oxide and bronchial responsiveness were assessed and nasal lavage fluid and induced sputum were also collected. Symptoms and body temperature were recorded before and after exposures.Following exposure to the pig barn, bronchial responsiveness, exhaled nitric oxide, sputum interleukin (IL)-6, nasal lavage cell count and IL-8 were increased to a greater extent in controls compared to farmers. The sputum IL-6 response was also attenuated in farmers after LPS challenge. The response shown by smokers following exposure to the pig barn was similar to that of controls regarding measurements of exhaled nitric oxide, IL-8 in nasal lavage and IL-6 in sputum, but more similar to farmers concerning bronchial responsiveness and the cell numbers present in nasal lavage. Sputum IL-8 showed a greater increase in smokers than in the other groups following LPS challenge.We conclude that individuals who are repeatedly exposed to organic material develop an adaptation to the effects of acute exposure to inhaled organic material.

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mentioning

confidence: 86%

Section: Occupational and Environmental Lung Diseasementioning

confidence: 99%

Repeated exposure to organic material alters inflammatory and physiological airway responses

Sundblad¹,

Schéele²,

Palmberg³

et al. 2009

European Respiratory Journal

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“…Because CS is known to contain detectable levels of LPS (40,41) and chronic LPS exposure is sufficient to induce both apoptosis and emphysematous changes in mice (42), LPS within CS may contribute causally to the CSE-induced apoptosis of HPAECs. Our previous work demonstrated that MIF is an endogenous determinant of endothelial cell sensitivity to LPSinduced apoptosis (21).…”

Section: Discussionmentioning

confidence: 99%

p53 Mediates Cigarette Smoke–Induced Apoptosis of Pulmonary Endothelial Cells

Damico

Simms

Kim

et al. 2011

Am J Respir Cell Mol Biol

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Exposure to cigarette smoke (CS) is the most common cause of emphysema, a debilitating pulmonary disease histopathologically characterized by the irreversible destruction of lung architecture. Mounting evidence links enhanced endothelial apoptosis causally to the development of emphysema. However, the molecular determinants of human endothelial cell apoptosis and survival in response to CS are not fully defined. Such determinants could represent clinically relevant targets for intervention. We show here that CS extract (CSE) triggers the death of human pulmonary macrovascular endothelial cells (HPAECs) through a caspase 9-dependent apoptotic pathway. Exposure to CSE results in the increased expression of p53 in HPAECs. Using the p53 inhibitor, pifithrin-a (PFT-a), and RNA interference (RNAi) directed at p53, we demonstrate that p53 function and expression are required for CSE-mediated apoptosis. The expression of macrophage migration inhibitory factor (MIF), an antiapoptotic cytokine produced by HPAECs, also increases in response to CSE exposure. The addition of recombinant human MIF prevents cell death from exposure to CSE. Further, the suppression of MIF or its receptor/binding partner, Jun activation domain-binding protein 1 (Jab-1), with RNAi enhances the sensitivity of human pulmonary endothelial cells to CSE via a p53-dependent (PFT-a-inhibitable) pathway. Finally, we demonstrate that MIF is a negative regulator of p53 expression in response to CSE, placing MIF upstream of p53 as an antagonist of CSE-induced apoptosis. We conclude that MIF can protect human vascular endothelium from the toxic effects of CSE via the antagonism of p53-mediated apoptosis.

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“…The following environmental exposures were selected as proxy measurements of high microbial exposure or infections: 1) siblings (number of older siblings present at birth: 0; 1; 2 or more); 2) day-care (day-care in first year of life; o4 h per week versus no day-care); 3) dog present in first year of life; 4) cat present in first year of life; 5) intrauterine smoke exposure in the last 3 months of pregnancy; and 6) environmental tobacco smoke exposure at home in the first year of life (tobacco smoke contains high levels of endotoxin [17]). …”

Section: Environmental Exposuresmentioning

confidence: 99%

Toll-like receptors and microbial exposure: gene-gene and gene-environment interaction in the development of atopy

Reijmerink¹,

Kerkhof²,

Bottema³

et al. 2011

European Respiratory Journal

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Environmental and genetic factors contribute to atopy development. High microbial exposure may confer a protective effect on atopy. Toll-like receptors (TLRs) bind microbial products and are important in activating the immune system.To assess whether interactions between microbial exposures and genes encoding TLRs (and related genes) result in atopy, genes, environmental factors and gene-environment interactions of 66 single-nucleotide polymorphisms (SNPs) of 12 genes (TLR 1-6, 9 and 10, CD14, MD2, lipopolysaccharide-binding protein (LBP) and Dectin-1), and six proxy parameters of microbial exposure (sibship size, pets (three different parameters), day-care and intrauterine and childhood tobacco smoke exposure) were analysed for association with atopic phenotypes in 3,062 Dutch children (the Allergenic study).The presence of two or more older siblings increased the risk of developing high total immunoglobulin (Ig)E levels at different ages. This risk increased further in children aged 1-2 yrs carrying the minor allele of TLR6 SNP rs1039559. Furthermore, novel two-and three-factor genegene and gene-environment interactions were found (e.g. between sibship size, day-care and LBP SNP rs2232596).Larger sibship size is associated with increased total IgE levels. Furthermore, complex two-and three-factor interactions exist between genes and the environment. The TLRs and related genes interact with proxy parameters of high microbial exposure in atopy development.

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Tobacco smoking increases dramatically air concentrations of endotoxin

Cited by 92 publications

References 9 publications

Repeated exposure to organic material alters inflammatory and physiological airway responses

Repeated exposure to organic material alters inflammatory and physiological airway responses

p53 Mediates Cigarette Smoke–Induced Apoptosis of Pulmonary Endothelial Cells

Toll-like receptors and microbial exposure: gene-gene and gene-environment interaction in the development of atopy

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