Exposure of cotton workers in an experimental cardroom with reference to airborne endotoxins.

Rylander, Ragnar; Haglind, Per

doi:10.1289/ehp.866683

Cited by 33 publications

(7 citation statements)

References 17 publications

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“…Historically, however, the study of organic dust-related disease has focused on acute airway responses, including chest tightness, cross-shift drops in forced expiratory volume in 1 s (FEV 1 ), and airway hyperresponsiveness. These acute airway responses may even be observed in healthy volunteers exposed for a short time in model cardrooms (52), or when exposed to extracts of grain dust (53). However, manifestations of a COPD-like presentation can appear after several years of exposure (5).…”

Section: Discussionmentioning

confidence: 99%

Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis

Brass

Hollingsworth²,

Cinque³

et al. 2008

Am J Respir Cell Mol Biol

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Lipopolysaccharide (LPS) is ubiquitous in the environment. Recent epidemiologic data suggest that occupational exposure to inhaled LPS can contribute to the progression of chronic obstructive pulmonary disease. To address the hypothesis that inhaled LPS can cause emphysema-like changes in mouse pulmonary parenchyma, we exposed C57BL/6 mice to aerosolized LPS daily for 4 weeks. By 3 days after the end of the 4-week exposure, LPS-exposed mice developed enlarged airspaces that persisted in the 4-week recovered mice. These architectural alterations in the lung are associated with enhanced type I, III, and IV procollagen mRNA as well as elevated levels of matrix metalloproteinase (MMP)-9 mRNA, all of which have been previously associated with human emphysema. Interestingly, MMP-9-deficient mice were not protected from the development of LPS-induced emphysema. However, we demonstrate that LPS-induced airspace enlargement was associated with apoptosis within the lung parenchyma, as shown by prominent TUNEL staining and elevated cleaved caspase 3 immunoreactivity. Antineutrophil antiserum-treated mice were partially protected from the lung destruction caused by chronic inhalation of LPS. Taken together, these findings demonstrate that inhaled LPS can cause neutrophil-dependent emphysematous changes in lung architecture that are associated with apoptosis and that these changes may be occurring through mechanisms different than those induced by cigarette smoke.

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Section: Discussionmentioning

confidence: 99%

Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis

Brass

Hollingsworth²,

Cinque³

et al. 2008

Am J Respir Cell Mol Biol

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“…It has been suggested that virus infection is capable of overriding inhalation‐induced IgE isotype tolerance and promoting airway allergic responses [ 30]. Endotoxins from the cell wall of Gram‐negative bacteria have been also implicated as etiological agents in the induction of acute and chronic respiratory symptoms, including bronchoconstriction and bronchial hyperreactivity [ 33, 34]. In the current study, we demonstrated that airborne endotoxins, which exist frequently in the subtropical area, can also break inhalation‐induced IgE isotype tolerance and promote airway‐allergic responses.…”

Section: Discussionmentioning

confidence: 99%

Airborne endotoxin exposure and the development of airway antigen‐specific allergic responses

Wan

Lin

2000

Clin Experimental Allergy

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“…These effects were again antagonized by propranolol and thus also appear to be mediated by an action on P-adrenoceptors. Eosinophil accumulation in the bronchial lumen is one of the hallmarks of asthma (Horn et al, 1975;Venge, 1985), while neutrophil accumulation is characteristic of other forms of inflammation (Rylander & Haglind, 1986;Thompson et al, 1989). Furthermore, eosinophil and neutrophil accumulation in the airways have been linked to nocturnal asthma (Martin et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Inhibition by salmeterol of increased vascular permeability and granulocyte accumulation in guinea‐pig lung and skin

Whelan

Johnson

1992

British J Pharmacology

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1. The long-acting P2-adrenoceptor agonist, salmeterol has been evaluated for its anti-inflammatory effects in the guinea-pig lung and skin. 2. Salmeterol, administered in bronchodilator doses to conscious guinea-pigs by both oral (0.01-1.0 mg kg-') and inhaled (nebulizer concentration, 0.001-1.0 mg ml-') routes, inhibited histamineinduced plasma protein extravasation (PPE) into the airway lumen. 3. Inhibition of PPE by salmeterol was long-lasting (>6 h) and was inhibited by prior administration of propranolol (1 mg kg-1, s.c.), indicating an effect mediated by P-adrenoceptors. 4. Inhaled salbutamol (nebulizer concentration, 0.00 1-1.0 mg ml-') also inhibited PPE in guinea-pig lung but, in contrast to salmeterol, this effect was short-lived with substantial loss of activity 2 h after administration. 5. Inhaled salmeterol (0.1 mg ml-') and salbutamol (1.0mg ml-') inhibited the accumulation of neutrophils in guinea-pig lung in response to lipopolysaccharide (100pgml-'). Salmeterol, but not salbutamol, inhibited the infiltration of eosinophils into the airway lumen in response to platelet activating factor (100 Lgml-'). These effects of salmeterol were blocked by prior administration of propranolol (5 mg kg-', s.c.), indicating that they were also P-adrenoceptor-mediated.6. Oral salmeterol (10mg kg-', p.o.), but not salbutamol (10 and 100mg kg-', p.o.), inhibited zymosan-induced granulocyte accumulation and PPE in guinea-pig skin. Lower doses of salmeterol (0.1 and 1 mg kg-') inhibited PPE, but not granulocyte accumulation. The effects of salmeterol were blocked by prior administration of propranolol (1mgkg-', s.c.). Both salmeterol and salbutamol inhibited histamine-induced PPE in guinea-pig skin.7. Intradermal salmeterol (10-'mol per site), but not salbutamol, was also effective in inhibiting zymosan-induced granulocyte accumulation and PPE in guinea-pig skin. 8. It is concluded that salmeterol, at bronchodilator doses in the guinea-pig, inhibits granulocyte accumulation and PPE, possibly by an action on the vasculature. As this profile of activity is not shared by the shorter-acting compound, salbutamol, it would seem that anti-inflammatory activity is associated with P-adrenoceptor agonism of long duration. The implications of these findings for the use of salmeterol in the treatment of bronchial asthma are discussed.

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Exposure of cotton workers in an experimental cardroom with reference to airborne endotoxins.

Cited by 33 publications

References 17 publications

Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis

Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis

Airborne endotoxin exposure and the development of airway antigen‐specific allergic responses

Inhibition by salmeterol of increased vascular permeability and granulocyte accumulation in guinea‐pig lung and skin

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