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Biomedical subjects

R Rylander

Publications and source records attributed to R Rylander.

At least 127 records · Page 7Linked to original sources
PubMed1988

Plant constituents of cotton dust and lung effects after inhalation.

Experiments were performed to assess pulmonary reactions after inhalation of cotton dusts with different levels of tannins, terpenoid aldehydes and bacterial endotoxins. Guinea-pigs were exposed to cotton dust. Free lung cells were obtained by lavage 24 h later. A dose-response relationship was found between the number of neutrophils and the amount of endotoxin in the dust. No influence of terpenoid aldehyde or tannin levels could be detected. Cotton mill workers were exposed to dust from glanded and glandless cottons in an experimental cardroom. The average decreases in forced expiratory volume in one second (FEV1) over the workday after carding the two cottons were the same, although levels of dust, tannin or terpenoid aldehydes were different. The level of airborne endotoxin was, however, equal. The results support observations from other studies on the importance of endotoxin for the development of the acute reactions observed after cotton dust exposure.

Animals↗
PubMed1987

The role of endotoxin for reactions after exposure to cotton dust.

Gram-negative bacteria and their endotoxins are present on all parts of the cotton plant and occur in large numbers after rain or frost. Endotoxins activate pulmonary macrophages that in turn recruit neutrophils into the airways. Platelets accumulate in pulmonary capillaries. The presence of these cells allows for the initiation of acute and chronic inflammation. Dose-response relationships have been demonstrated between endotoxin and fever, chest tightness, and reduction in air flow (bronchoconstriction) in cotton workers. Limited data suggest that after cotton dust exposure, other symptoms, such as airway hyperreactivity and chronic inflammation, are also related to the endotoxin exposure. Tentative thresholds for airborne endotoxins are presented.

Byssinosis↗
PubMed1987

Interstitial and free lung cells in acute inflammation in the guinea-pig.

Different cell types were studied in bronchoalveolar lavage fluid (BAL) and solid lung tissue of guinea-pigs. Whereas alveolar macrophages (AM) and eosinophils predominated in BAL, the proportion of AM and lymphocytes was highest in the lung tissue. After an inhalation exposure to LPS, the number of neutrophils increased rapidly in the lung tissue reaching a maximum after 4 hours, and more slowly in the airways reaching a maximum after 24 hours. This suggests that other mechanisms than secretion of chemotactic factors from AM, shown to be active up to 4 hours after exposure, are responsible for the later phase of the neutrophil invasion into the airways. Passive migration or other mediators may be involved.

Animals↗
PubMed1987

The involvement of platelet activating factor in endotoxin-induced pulmonary platelet recruitment in the guinea-pig.

1 Exposure of conscious guinea-pigs to an aerosol of endotoxin (25-100 micrograms ml-1) resulted in a dose-related, progressive accumulation of platelets in the thoracic region. Accumulation of 111indium oxine labelled erythrocytes was not observed following exposure to an aerosol of endotoxin (50 micrograms ml-1). 2 Pretreatment of guinea-pigs with the selective platelet activating factor (Paf)-antagonists. CV-3988 or brotizolam resulted in a dose-related inhibition of endotoxin-induced pulmonary platelet recruitment. Pretreatment of guinea-pigs with the selective Paf-antagonist BN 52021 resulted in significant inhibition of endotoxin-induced pulmonary platelet recruitment, although the effects of BN 52021 were not dose-related. 3 Pretreatment of guinea-pigs with indomethacin at doses known to inhibit cyclo-oxygenase did not inhibit endotoxin-induced pulmonary platelet recruitment, whereas higher doses of indomethacin produced a reduction in platelet recruitment in the lung. 4 Pretreatment of guinea-pigs with the anticoagulant heparin and the prostacyclin analogue ZK 36374 inhibited endotoxin-induced platelet recruitment. 5 These observations suggest that endotoxin-induced pulmonary platelet recruitment in the guinea-pig is secondary to the release of platelet activating factor, but not to cyclo-oxygenase products of arachidonic acid and may also involve activation of the coagulation cascade.

Animals↗
PubMed1987

Byssinosis in carpet weavers exposed to wool contaminated with endotoxin.

All the 303 full time day workers in a carpet weaving factory were submitted to a physical examination, chest radiography, and vitalograph test, and answered a respiratory questionnaire. Fifty four healthy non-exposed subjects served as controls. Dust concentrations and concentrations of bacterial endotoxin were measured. Of the 303 workers, 259 (85.5%) had airway symptoms and 62 (20.5%) had maximum mid-expiratory flow (MMF) values of less than 60% compared with 9.2% of the controls. The symptoms in 68 workers (22%) were compatible with byssinosis and 36 of these workers underwent vitalography before starting work and after four hours work on Mondays when significant reductions of their FEV1 and MMF were found. Twenty one of these 36 workers were tested on Tuesday and no differences in these measurements were found between measurements before work started and four hours later. The airborne dust concentrations in the factory were high and bacterial endotoxin was found. These findings suggest that a large number of workers in this carpet weaving factory suffer from a disease indistinguishable from byssinosis even though wool is used almost exclusively, the only cotton being the warp. The finding of endotoxin together with the absence of cotton confirms the theory that "byssinosis" is due to bacterial endotoxin rather than to cotton per se.

Adult↗
PubMed1987

Inhalation of endotoxin stimulates alveolar macrophage production of platelet-activating factor.

The production of PAF was studied in alveolar macrophages (AM) and neutrophils recovered by bronchial lavage from guinea pigs exposed to aerosolized bacterial endotoxin (lipopolysaccharide, LPS). The amount of cell-associated PAF was estimated by measuring serotonin release from rabbit platelets. An increased and dose-related production was found in AM for as long as 2 h after a 40-min exposure. No production was detectable after 4 h. Prolonging the exposure did not prolong the response. When a second exposure was given, no PAF could be detected until the time interval between the 2 exposures was 72 h. The amount of neutrophils in lung lavage fluid was elevated about 100 times at 4 h after the exposure, but only a minor PAF production was found in these cells. In view of the role of LPS-contaminated dusts for the development of human lung disease, particularly airway constriction, the role of PAF needs to be further investigated.

Administration, Inhalation↗
PubMed1987

Lysosomal enzyme activity and fibroblast stimulation of lavage from guinea pigs exposed to silica dust.

Guinea pigs were exposed to silica dust for 3 weeks and examined up to 1 year thereafter. The activity of several lysosomal enzymes in lung lavage fluid (LLF) increased from 8 weeks after cessation of exposure whereas the level in aveolar macrophages decreased. Collagen synthesis in fibroblast cultures exposed to LLF was also increased except at 24 weeks after exposure. The results indicate that 8 weeks and later after cessation of exposure to silica dust there are cellular changes in the lung which can be related to the exposure, although typical silicotic lesions were not observed till 1 year after the exposure.

Acetylglucosaminidase↗
PubMed1987

Kinetics of inhaled lipopolysaccharide in the guinea pig.

The kinetics of endotoxin in the airway and the blood was studied after an inhalation exposure using guinea pigs. The amounts of endotoxin in the pulmonary lavage fluid, and in arterial and venous blood were determined. Forty minutes after the start of exposure to 400 micrograms/m3 of Escherichia coli 026:B6-LPS, 7.7 +/- 2.9 ng/ml of lipopolysaccharide (LPS) could be demonstrated in the pulmonary lavage fluid, and 60 minutes afterwards, the amount was 4.9 +/- 1.4 ng/ml. In the arterial blood, the amounts at 10 and 40 minutes of exposure, and 60 minutes afterwards were 21.2 +/- 23.8 pg/ml, 29.2 +/- 31.8 pg/ml, and 1.1 +/- 1.0 pg/ml, respectively. There was no significant difference of LPS content in the arterial and venous blood. The results demonstrate that the lung is a potent barrier for penetration of endotoxins into the body. The experimental model enables studies of how other exposures such as mineral dusts, tobacco smoke, or viral or bacterial infections might affect this defense.

Administration, Inhalation↗
PubMed1987

Occupational exposure and lung function measurements among workers in swine confinement buildings.

Previous studies have demonstrated that air in swine confinement buildings contains large amounts of dusts, highly contaminated with microorganisms and bacterial endotoxin. A study was undertaken to investigate the respiratory function of workers before and after the work shift in swine confinement buildings. Questionnaires were mailed to workers on swine farms. Dust levels were measured by personal sampling, and the micro-flora in the dust was determined. Work-related symptoms from the lung were frequent. Several workers who were smokers had forced expiratory volume in 1 second (FEV1) values lower than expected when they started work. Among a group of life-long nonsmoking workers the baseline forced vital capacity and FEV1 were not decreased. Changes in the FEV1 over the working shift were generally not found. It is suggested that exposure to dust in swine confinement buildings may lead to respiratory impairment but further studies on larger population samples and different exposure conditions are required.

Air Microbiology↗
PubMed1986

Lung diseases caused by organic dusts in the farm environment.

Organic dusts present in the farm environment may cause a series of lung cell reactions involving inflammation and immune responses. Clinical diseases related to this exposure and based on the inflammation may be divided into acute and chronic inflammation. These can be accompanied by airway hypersensitivity. Individual clinical cases often present atypical or mixed symptoms that must be recognized as a work-related disease.

Alveolitis, Extrinsic Allergic↗
PubMed1986

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

Workers from cotton mills were exposed to cotton dust during carding in an experimental cardroom. Cotton from different geographical locations with varying amounts of endotoxin were used. Exposure levels ranged from 0.6 to 3.6 mg dust/m3 (from a vertical elutriator) and from 0.1 to 8.0 micrograms/m3 of endotoxin. No relationship was found between the decrease in FEV1 over the workshift and the amount of airborne dust. Airborne endotoxin correlated with the decrease in FEV1 and the increase in blood neutrophils. The FEV1 decrease was more pronounced among smokers. The data suggest that the amount of airborne endotoxin determines the risk for development of the acute symptoms in the byssinosis syndrome.

Air Pollutants, Occupational↗
PubMed1985

Free lung cell phagocytosis and lysosomal enzyme activity after inhalation of lipopolysaccharide in guinea-pigs.

Free lung cells were studied in guinea-pigs different times after an inhalation exposure to bacterial endotoxin yielding a dose of about 1 microgram/animal. After exposure the number of alveolar macrophages (AM) and neutrophils was increased. The phagocytosis capacity of the lung was increased, mainly due to the influx of neutrophils. The activity of N-acetyl-beta-D-glucosaminidase from exposed animals was decreased in AM cell cultures and increased in lavage fluid 2 hours and later after exposure. Cathepsin D activity was also decreased in AM cell cultures but did not change in lavage fluid. Lactate dehydrogenase was increased in lung lavage fluid. The results show that LPS inhalation activates AM and that increased amounts of lysosomal enzymes are present in the airways.

Acetylglucosaminidase↗
PubMed1985

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages.

Guinea-pigs were exposed to an aerosol of bacterial endotoxin (lipopolysaccharide, LPS). The free lung cell response and alveolar macrophage (AM) chemotaxis were studied. Neutrophils from guinea-pig blood gave larger migration responses than those obtained by intraperitoneal glycogen stimulation or human neutrophils. An increase in the number of neutrophils in the airways was found with a peak at 12-24 hours after exposure. In animals pre-treated with LPS inhalation for 4 months, the reaction was of shorter duration and smaller magnitude. AM showed in vitro chemotactic activity up to 4 hours after exposure; no difference was found in pre-treated animals. The results suggest that the neutrophil invasion in the airways after LPS is dependent on two mechanisms, the initial being AM chemotaxis, which is not modified by pre-exposure to LPS, and another unknown factor, which is modified by pre-exposure to LPS.

Aerosols↗
PubMed1985

Comparative toxicity studies between bacterial lipopolysaccharide (endotoxin) and N-formyl methionyl peptide as factors in the pathogenesis of byssinosis.

Comparative in vivo and in vitro studies were made on bacterial lipopolysaccharide (LPS) and the chemotactic peptide NF-Met-Leu-Phe with a view toward studying their possible role in the pathophysiology of byssinosis. In contrast to LPS, chemotactic peptides did not cause Limulus amebocyte lysate gelation, nor did they induce the release of endogenous pyrogen. Inhalation of LPS caused a peripheral leukocytosis in rabbits 30 min after aerosol administration, whereas peptide inhalation caused a significant leukopenia in the same period. Cellular analysis of guinea pig bronchial lavages after LPS aerosol challenge revealed immediate decreases in all cell types, with subsequent, large increases of macrophages and granulocytes 4-24 h after aerosolization. Inhalation challenge with NF-Met-Leu-Phe induced no significant cellular changes. It was concluded that it is unlikely that these microbial products could be confused with each other when administered in pure form by the inhalation route.

Animals↗