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S Von Essen

Publications and source records attributed to S Von Essen.

10 recordsLinked to original sources
PubMed1997

The role of endotoxin in grain dust exposure and airway obstruction.

Grain dust exposure is a common cause of respiratory symptoms in grain workers, feed mill employees, and farmers. Many of these workers develop wheezing and acute and chronic bronchitis symptoms, which can be associated with obstructive changes on pulmonary function testing. It has recently been demonstrated that grain dust exposure causes neutrophilic airways inflammation and systemic symptoms related to release of interleukin-1, tumor necrosis factor, interleukin-6, and other mediators of inflammation. Although grain dust is a heterogenous substance, endotoxin has received the greatest amount of attention as a possible cause of the airway inflammation that occurs after grain dust exposure. Although endotoxin undoubtedly causes a portion of the changes seen after grain dust exposure, it is becoming clear that other substances play a role as well.

Agricultural Workers' Diseases↗
PubMed1997

Neurogenic plasma exudation mediates grain dust-induced tissue injury in vivo.

The purpose of this study was to determine whether an aqueous extract of grain sorghum dust (GDE) elicits neurogenic plasma exudation in the oral mucosa in vivo. Using intravital microscopy, we found that GDE elicited significant, concentration-dependent leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the hamster cheek pouch (P < 0.05). The selective, nonpeptide neurokinin(1) (substance P) receptor antagonists, CP-96,345 and RP-67580, but not the 2R,3R enantiomer CP-96,344, significantly attenuated GDE-induced leaky site formation and increase in clearance of FITC-dextran (P < 0.05). Indomethacin had no significant effects on GDE-induced responses. CP-96,345 had no significant effects of adenosine-induced leaky site formation and increase in clearance of FITC-dextran from the cheek pouch. We conclude that GDE elicits neurogenic plasma exudation from the oral mucosa in vivo. We suggest that this process is one mechanism whereby grain sorghum dust elicits immediate oral mucosa inflammation in vivo.

Adenosine↗
PubMed1995

Cigarette smoke stimulates release of neutrophil chemotactic activity from cultured bovine bronchial epithelial cells.

1. Recruitment of neutrophils into the airway is a prominent feature of chronic bronchitis, a syndrome often associated with exposure to cigarette smoke. Since bronchial epithelial cells are the 'first' lung cells to come into contact with smoke, these cells may be responsible for neutrophil recruitment into the airway by release of neutrophil chemotactic activity in response to cigarette smoke. 2. To evaluate this hypothesis, we prepared bovine bronchial epithelial cells and measured their ability to release neutrophil chemotactic activity following exposure to cigarette smoke. Bronchial epithelial cells were prepared by overnight digestion with protease, filtered through 100-microns Nitex mesh and resuspended in Dulbecco's modified Eagle medium supplemented with 10% fetal calf serum and antibiotics and cultured at 2 x 10(6) cells in 2 ml of medium in 35-mm culture dishes. After 4 days, dishes were rinsed and refed with medium without fetal calf serum and incubated with and without 1:10 diluted smoke extract for 6 h at 37 degrees C. The neutrophil chemotactic activity of the supernatant fluids was measured by the blindwell chamber technique. 3. Cigarette smoke itself added to medium did not stimulate chemotaxis. In contrast, cigarette smoke did stimulate the release of neutrophil chemotactic activity from bovine bronchial epithelial cells [15 +/- 3 (control) versus 74 +/- 5 (smoke), P < 0.01]. 4. This neutrophil chemotactic activity was dialysable, pepsin and acid stable, heat sensitive and lipid extractable. Sephadex G-75 column chromatography demonstrated two peaks of neutrophil chemotactic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Animal models.

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Animals↗
PubMed1991

Endotoxin stimulates bronchial epithelial cells to release chemotactic factors for neutrophils. A potential mechanism for neutrophil recruitment, cytotoxicity, and inhibition of proliferation in bronchial inflammation.

To test the effect of endotoxin on bronchial epithelial cells (BEC), BEC were isolated from bovine lungs and cultured in the presence of bacterial endotoxin. The BEC culture supernatant fluids were harvested, and neutrophil chemotactic activity (NCA) was determined with a blindwell chamber technique; cytotoxicity determined by lactate dehydrogenase release and BEC proliferation determined by Coulter counting. Endotoxin caused a dose- and time-dependent release of NCA from BEC cultures compared with media alone (82.3 +/- 8.1 vs 12.0 +/- 3.1 cells/high power field, p less than 0.001). To further characterize this activity, reverse phase HPLC analysis of release eicosanoid metabolites after [3H]arachidonic acid incorporation was performed. Endotoxin stimulated the release of the neutrophil chemoattractants, leukotriene B4 and 12-hydroxyeicosatetraenoic acids. Endotoxin also resulted in a dose and time dependent release of lactate dehydrogenase (42.9 +/- 4.2 vs 20.2 +/- 2.2 U/liter, p less than 0.001) although higher doses were required to cause cytotoxicity than to stimulate chemotaxis. Finally, endotoxin resulted in a dose dependent inhibition of BEC proliferation (176 x 10(3) +/- 16 x 10(3) vs 1,080 x 10(3) +/- 38 x 10(3) cells/ml measured at day 14, p less than 0.001). These data suggest that bacterial release of endotoxin may contribute to the pathophysiologic changes observed in bronchial inflammation by stimulating BEC to release NCA, denuding airway epithelium by causing cytotoxicity of BEC, and inhibiting epithelial repair by inhibiting BEC proliferation.

Animals↗
PubMed1990

Complete resolution of roentgenographic changes in a patient with pulmonary histiocytosis X.

A smoker presented with pleuritic chest pain and was found to have reticulonodular interstitial opacities on chest x-ray film. Open lung biopsy revealed changes consistent with histiocytosis X, a disease seen almost exclusively in smokers. Smoking cessation was recommended, and the patient complied. A chest x-ray film taken nearly three years later revealed complete resolution of the radiographic abnormalities. It is proposed that smoking cessation may be related to the improvement in this patient's chest x-ray film findings, and that it should be recommended for all patients with pulmonary histiocytosis X.

Adult↗
PubMed1990

Organic dust toxic syndrome: an acute febrile reaction to organic dust exposure distinct from hypersensitivity pneumonitis.

Organic dust toxic syndrome is a term recently coined to describe a noninfectious, febrile illness associated with chills, malaise, myalgia, a dry cough, dyspnea, headache and nausea which occurs after heavy organic dust exposure. Organic dust toxic syndrome shares many clinical features with acute farmer's lung and other forms of hypersensitivity pneumonitis, including the presence of increased numbers of neutrophils in bronchoalveolar lavage. However, organic dust toxic syndrome differs from acute hypersensitivity pneumonitis in several respects: the chest X-ray does not show infiltrates, severe hypoxemia does not occur, prior sensitization to antigens in the organic dust is not required and there are no known sequelae of physiological significance, such as the recurrent attacks and the pulmonary fibrosis which may be seen with chronic hypersensitivity pneumonitis. Organic dust toxic syndrome is thought to be much more common than farmer's lung. It is important for clinical and investigational purposes that organic dust toxic syndrome be distinguished from acute farmer's lung.

Acute Disease↗
PubMedDate not supplied

In vivo and in vitro methods for evaluating airways inflammation: implications for respiratory toxicology.

The lung is frequently the target of injury for toxic exposures. Often these exposures lead to significant disease. Assessment of toxic exposures to the lung, however, may be made using both in vitro and in vivo methods. Recent advances in respiratory cell biology have made possible in vitro analyses of the interactions between airway cells and potential toxins. In addition, the lung can be sampled in vivo using bronchoscopy and bronchoalveolar lavage. This opens up the possibility of assessing potential toxins prior to the development of clinically significant disease. Together, these advancing methodologies promise new potential for the assessment and evaluation of toxic exposures to the lung.

Air Pollutants↗