Aspects on the alveolar accumulation of T cells in sarcoidosis.
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Bronchoalveolar Lavage Fluid↗
Biomedical subjects
A Eklund
Publications and source records attributed to A Eklund.
Fosfomycin/metronidazole compared with doxycycline/metronidazole for the prophylaxis of infection after elective colorectal surgery. A randomised double-blind multicentre trial in 517 patients.
OBJECTIVE: To find out if fosfomycin together with metronidazole was any better than doxycycline with metronidazole for the prophylaxis of infection before elective colorectal operations. DESIGN: Multicentre, double blind, random control trial. SETTING: Nine Swedish hospitals. SUBJECTS-559 patients admitted for elective colorectal operations. INTERVENTIONS: Fosfomycin 8 g and metronidazole 1 g before operation and fosfomycin 8 g eight hours afterwards, or doxycycline 400 mg and metronidazole 1 g before operation, and placebo eight hours afterwards. MAIN OUTCOME MEASURES: Incidence of all types of infection, mortality, and side effects. RESULTS: There were no significant differences between the groups for any of the outcome measures studied, the overall abdominal infection rates (wound, deep, and septicaemia) being 4.6% and 7.4%, and the remote infection rates (pneumonia, urinary tract, and central venous line) 15.1% and 12.8%, respectively. Of the predictors studied, only duration of operation was significantly related to risk of infection. CONCLUSION: The combination of fosfomycin and metronidazole was as safe and effective as that of doxycycline and metronidazole in preventing infections after elective colorectal operations.
Aged↗
Endocytosis of cigarette-smoke condensate by rabbit alveolar macrophages in vitro measured as fluorescence intensity.
It has previously been shown that alveolar macrophages (AMs) from smokers have increased fluorescence compared to AMs from nonsmokers. In the present investigation, AMs lavaged from rabbits were exposed to a cigarette-smoke condensate (CSC) in order to study its influence on the fluorescence of AMs. Flow cytofluorometry was used. Alveolar cells exposed to 0.01% of CSC showed a fluorescence which increased with higher concentrations of the CSC. Incubation with CSC for 5 min was enough to give a significant rise (p less than 0.001) in cell fluorescence compared to controls. After incubating fluorescent cells with untreated non-fluorescent AMs, fluorescent material was distributed to the non-fluorescent AMs within 30 min. Further more, fluorescence decreased when exposed cells were cultured in CSC-free medium. When incubating CSC with blood leucocytes, an almost threefold increase in fluorescence was observed among the phagocytic cells at 37 degrees C compared to 4 degrees C, whereas the fluorescence in the non-phagocytic cell population only showed a minor enhancement. Endocytosis of fluorescent material in CSC can explain the strong fluorescence seen in AMs from smokers. Exocytosis and re-endocytosis of the material by new AMs may explain the slow decline in the fluorescence of AMs observed after cessation of smoking.
Animals↗
Quenching of intracellular autofluorescence in alveolar macrophages permits analysis of fluorochrome labelled surface antigens by flow cytofluorometry.
We report a new technique in which the autofluorescence of alveolar macrophages from smokers is quenched by crystal violet. This technique permits immunostaining of surface antigens of these cells and enables the stained cells to be analysed by flow cytofluorometry. The variable solubility of crystal violet makes it important to characterize the crystal violet solution by its quenching properties and not rely on the assumed concentration of dissolved dye. High concentrations of crystal violet lowered the number of cells and gave a decreased amount of surface antigen (CD11b). However, a lower concentration of crystal violet could be used if the cells were fixed with paraformaldehyde (4%) and the membranes were permeabilized with n-octyl-beta-D-glucopyranoside (0.6%). Using a phagocytic model with FITC-conjugated particles we were able to show that this treatment gave an efficient permeabilization of phagolysosomal membranes.
Antigens, Surface↗
The effects of dietary protein on the fatty acid composition and delta 6 desaturase activity of rat hepatic microsomes.
Recently, significant differences between rats fed a casein diet and rats fed a soybean protein diet have been observed in hepatic phospholipid fatty acid patterns (Sjöblom, L., and Eklund, A., Biochim. Biophys. Acta 1004, 187-192, 1990). The influence of these two diets on the delta 6 desaturase activity was investigated in the present study because the hepatic desaturase system is a source of unsaturated fatty acids. The rats fed a casein diet showed higher desaturase activity than those fed soybean protein when using either linoleic acid (P less than 0.005) or oleic acid (P less than 0.05) as substrates. The phosphatidylcholine fraction of hepatic microsomes showed increases in oleic acid (P less than 0.005) and 20:3 omega 9 (P less than 0.001) levels as well as decreases in stearic acid (P less than 0.001), linoleic acid (P less than 0.005) and arachidonic acid (P less than 0.005) levels in rats which were fed casein rather than soybean protein. Similar differences between the two groups were also observed in the phosphatidylethanolamine and phosphatidylinositol fractions. These data indicate that the qualitative properties of the dietary protein source may influence the fatty acid pattern of rat hepatic microsomes by interfering with delta 6 desaturase activity.
Animals↗
Plasma very low density lipoproteins from male rats fed casein or soybean protein diets: a comparison of fatty acid composition and influence on prostanoid production.
In studies with male rats fed for 4 wk semipurified diets containing olive oil and casein or soybean protein, protein-dependent effects were observed in the fatty acid composition of the VLDL lipids, especially with regard to the pattern of polyunsaturated fatty acids. Compared with VLDL from rats fed soybean protein diet (S-VLDL), VLDL from casein-fed rats (C-VLDL) contained a greater level of oleic acid, and a reduced level of linoleic acid and arachidonic acid, in the phosphatidylcholine fraction. The proportion of 5,8,11-eicosatrienoic acid, 20:3 (n-9), varied among the different lipid classes. The highest concentration of this fatty acid (13% by weight of total fatty acids) was observed in the phosphatidylinositol fraction of C-VLDL. The level of linoleic acid was approximately halved in the triacylglycerol and cholesteryl ester fractions of C-VLDL compared with S-VLDL. When mouse peritoneal macrophages were incubated with different concentrations of S-VLDL, a saturable accumulation of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) was observed in the cell medium. In contrast, very low levels of 6-keto-PGF1 alpha and TXB2 were observed in the cell medium of macrophages incubated with C-VLDL at different lipoprotein concentrations, suggesting that the composition of VLDL may play an important role in relation to cellular prostanoid metabolism.
6-Ketoprostaglandin F1 alpha↗
Distributions of transverse energy and forward energy in 16O- and 32S-induced heavy ion collisions at 60A and 200A GeV.
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Journal Article↗
Extracellular matrix components in bronchoalveolar lavage fluid in quartz exposed rats.
To investigate the long term effects of quartz, bronchoalveolar lavage (BAL) and analysis of lung silica were performed in rats (n = 20) one, four, and 12 months after exposure to intratracheally instilled crystalline silica. Total and relative concentrations of silica in the lungs were highest one month after exposure. At this time BAL fluid concentrations of total cells, macrophages, and lymphocytes increased five to 10-fold compared with saline instilled controls (n = 19). The number of polymorphonuclear cells (PMNs) increased about 200-fold. The increased number of PMNs persisted during the year. Furthermore, albumin and fibronectin concentrations increased continually during the year, about two to fivefold the values of controls. Hyaluronan, by contrast, increased during the four month period (about eightfold) but decreased after one year to the one month concentration. Phospholipids in BAL fluid, raised already after one month, remained high at one year. The findings suggest progressive damage of the alveolar and interstitial tissues. Moreover, the increases in components of the extracellular matrix capable of building fibrotic networks are in agreement with the microscopical findings of fibrosis. Because only total cells, macrophages, and albumin concentrations correlated weakly with the silica contents of the lung, it is unlikely that the relation between quartz burden and the reaction in the lung is simple.
Animals↗
Pulmonary reactions caused by welding-induced decomposed trichloroethylene.
This is the report of a welder who performed argon-shielded electric arc welding in an atmosphere containing trichloroethylene. He developed immediate respiratory symptoms, pulmonary edema 12 hours after exposure, and recurring dyspnea ten days after exposure. These pulmonary reactions might be explained by inhalation of decomposition products of trichloroethylene such as dichloroacetyl chloride and phosgene.
Dyspnea↗
Bronchoalveolar lavage fibronectin in patients with sarcoidosis: correlation to hyaluronan and disease activity.
Bronchoalveolar lavage was performed in 51 patients with sarcoidosis and in 21 healthy nonsmokers. The concentration of fibronectin was significantly higher (p less than 0.001) in lavage fluid from sarcoid patients (median 267 micrograms.l-1) than in that of controls (46 micrograms.l-1). Furthermore, a significantly higher concentration of fibronectin was found in patients with active disease than in those in whom the disease was inactive (p less than 0.001). In a six month follow-up perspective, patients with a progressive disease course had significantly higher levels of fibronectin than those who had a stable or regressive disorder (p less than 0.01). Correspondingly, lavage hyaluronan was higher (p less than 0.001) in sarcoid patients (55 micrograms.l-1) than in controls (9 micrograms.l-1) and higher (p less than 0.01) in those with active than in those with inactive disease. Patients with progressive disease had higher (p less than 0.01) concentrations of hyaluronan than those in whom the disease was stable. A significant correlation was found between lavage fibronectin levels and hyaluronan (r = 0.81, p less than 0.001). The percentage of mast cells was also higher in patients with active than in those with inactive disease (p less than 0.01) and higher in progressive than in stable sarcoidosis (p less than 0.001). Ten out of 10 patients with progressive disease had mast cells greater than or equal to 0.5%, hyaluronan greater than or equal to 50 micrograms.l-1 and fibronectin greater than or equal to 350 micrograms.l-1 compared to eight out of 41 patients with stable or regressive disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Inflammatory cell response in bronchoalveolar lavage fluid after nitrogen dioxide exposure of healthy subjects: a dose-response study.
The combination of environmental chamber exposure and bronchoalveolar lavage (BAL) was used to study the effects of the common air pollutant nitrogen dioxide (NO2). Eighteen healthy nonsmokers were exposed to NO2 during 20 min in an exposure chamber during light bicycle ergometer work. All subjects were examined with BAL at least 3 wks before exposure, as a reference. The subjects were re-examined with BAL, in groups of eight, 24 h after exposure to 4, 7 and 10 mg NO2.m.3 (2.25, 4.0 and 5.5 ppm), respectively. An inflammatory cell response was found after exposure to all concentrations. An increase in the number of lymphocytes in BAL fluid was observed after 7 and 10 mg.m.3 (p less than 0.05 and 0.02, respectively). An increase in the number of mast cells, that appears to be dose-dependent, was found after exposure to all concentrations. The proportion of lysozyme positive alveolar macrophages was elevated after exposure to 7 mg.m.3. The inflammatory mediators fibronectin, hyaluronan, angiotensin converting enzyme (ACE) and beta 2-microglobulin were unchanged by exposure. Due to the findings of inflammatory cell changes far below the peak exposure limits for work places in industrialized countries, 9-18 mg.m.3, the safety of these limits is questioned. Studies are in progress in our laboratory using BAL to evaluate the effects of repeated NO2 exposure.
Adult↗
Dietary protein and fatty acid composition of liver lipids in the rat.
In order to compare the effects of different sources of dietary protein on the fatty acid composition of phosphatidylcholines (PC), phosphatidylethanolamines (PE), phosphatidylinositols (PI), cholesteryl esters and triacylglycerols, male rats were fed for a 4-week period on cholesterol-free, or cholesterol-containing, diets based on casein, or soybean protein and olive oil. The most conspicuous difference observed was the occurrence of significantly higher levels of 5,8,11-eicosatrienoic acid, 20:3 (n - 9), in the different lipid classes of casein-fed, compared with soybean protein-fed, animals. In the PI fraction of livers from the groups of rats fed casein diet, this fatty acid amounted to between 9.9 and 13.3% by weight of the total fatty acids. Phospholipids from livers of casein-fed rats contained increased levels of oleic acid, 18:1 (n - 9) (in PC and PE) and reduced levels of stearic acid (18:0). Moreover, in this group of rats PI contained a reduced level of arachidonic acid, 20:4 (n - 6). A casein-related decrease in the linoleic acid, 18:2 (n - 6), content of PC and PE was observed only in the rats fed on cholesterol-free diet. Effects on the fatty acid composition were also observed in the triacyglycerol and cholesteryl ester fractions, in which the rats fed casein diet showed higher levels of palmitoleic acid, 16:1 (n - 7) (cholesterol-supplemented diet) and lower values for linoleic acid, than the soybean protein-fed rats.
Animals↗
Distribution of toxaphene, DDT, and PCB among lipoprotein fractions in rat and human plasma.
The distribution of 14C-toxaphene, 14C-DDT, and 14C-PCB among lipoprotein fractions was studied in vitro and in vivo using rat and human plasma. The association of these substances with rat plasma fractions was similar in both in vitro and in vivo experiments. Thirty-seven to fifty-two per cent of the total radioactivity was associated with the cholesterol-rich high density lipoproteins (HDL2, d = 1.075-1.21 g/ml) and 18-52% was recovered in the albumin-rich bottom fraction (BF, d greater than 1.21 g/ml). A time-dependent redistribution of the radioactivity from the lipoprotein fractions to the BF was also observed in the in vivo studies. In human plasma, the distribution of the three compounds was different and uncorrelated to the cholesterol level of the individual lipoprotein fractions. Toxaphene was almost equally distributed between BF (d greater than 1.21 ml), HDL (d = 1.063-1.21 g/ml) and low density lipoproteins (LDL, d = 1.006-1.063 g/ml) (26%, 27% and 29%, respectively), while only 18% appeared in the very low density lipoprotein (VLDL, d less than 1.006) fraction. In contrast, a large proportion of DDT and PCB radioactivity was recovered in the BF (52% and 62%, respectively) while only 38-48% was present in lipoprotein fractions. The complex nature of the interaction between xenobiotics and plasma lipoproteins is discussed.
Animals↗
Tissue accumulation of lipoprotein associated toxaphene in normo- and hypolipidemic mice.
Normo- and hypolipidemic mice were given a single i.v. injection of 14C-toxaphene associated with low density lipoprotein (LDL), high density lipoprotein (HDL) or dimethyl sulfoxide (DMSO). The tissue distribution of radioactivity was studied 20 min and 4 h after the application. In the normolipidemic mice at 20 min postinjection there was high uptake of the 14C-toxaphene preparations in the liver and adrenals followed after 4 h by a redistribution to the adipose tissues. In the hypolipidemic mice, proportionally less label accumulated initially in the liver and adrenals while more radioactivity was seen in the kidneys and heart. The radioactivity then redistributed to the liver with a very small uptake in the adipose tissue compared to the normolipidemic mice after 4 h. The results indicate that changes in the lipid pattern, e.g. hypolipidemic conditions, may influence the tissue distribution of lipophilic xenobiotics.
Animals↗
Hydrophobic surfactant-associated polypeptides: SP-C is a lipopeptide with two palmitoylated cysteine residues, whereas SP-B lacks covalently linked fatty acyl groups.
Pulmonary surfactant contains two hydrophobic polypeptides, SP-B and SP-C, with known amino acid sequences and with truncated subforms lacking the N-terminal residues. Treatment of SP-C with KOH releases fatty acids (palmitic acid to more than 85%) in molar ratios of 1.8-2.0 relative to the polypeptide. Furthermore, plasma-desorption mass spectrometry shows native SP-C of both the intact and truncated types to be monomers with masses about 500 units higher than those expected for the polypeptide chains. After treatment with KOH, trimethylamine, or dithioerythritol, the polypeptide masses are obtained. These results prove that native SP-C is a lipopeptide with two palmitoyl groups covalently linked to the polypeptide chain. The deacylation conditions, the presence of two cysteine residues in the polypeptide, and the absence of other possible attachment sites establish that the palmitoyl groups are thioester-linked to the two adjacent cysteine residues. In contrast, the major form of porcine SP-B is a dimer without fatty acid components. That SP-C is a true lipopeptide with covalently bound palmitoyl groups suggests possibilities for functional interactions. It gives a direct physical link between SP-C and surfactant phospholipid components. Long-chain acylation may constitute a means for association of proteins with membranes and could conceivably modulate the stability and biological activity of surfactant films.
Amino Acid Sequence↗
Beta-adrenoceptors in human alveolar macrophages isolated by elutriation.
1. beta-adrenoceptors on human alveolar macrophages obtained by bronchoalveolar lavage (BAL) from healthy smoking volunteers (n = 26) were characterized by studying cyclic AMP (cAMP) accumulation in intact macrophages evoked by adrenaline or isoprenaline, with or without appropriate antagonists and by radioligand binding to macrophage membranes, using [125I]-iodopindolol (125IPIN) as beta-adrenoceptor ligand. 2. In a second study, cAMP responses of alveolar macrophages to isoprenaline and PGE1 and of peripheral blood lymphocytes to isoprenaline were compared in smoking and non-smoking healthy volunteers (n = 9 + 9), as our initial studies were performed in smokers, due to their higher cell yield. 3. BAL yielded 47 +/- 23 x 10(6) cells in smokers and 12 +/- 6 x 10(6) cells in non-smokers with a recovery of 82 +/- 8% in the elutriation step (means +/- s.d.). The cell preparation consisted of 99.2 +/- 0.8% macrophages and their viability (trypan blue exclusion) was 97.5 +/- 5.2%. 4. Isoprenaline or adrenaline increased cAMP accumulation approximately 40-fold with or without the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX, 10(-4) M), which enhanced basal and stimulated cAMP accumulation approximately five-fold. Peak responses were seen after 2 min. EC50s for isoprenaline and adrenaline were 3-5 x 10(-7) M. Phentolamine did not alter responses to adrenaline, indicating absence of inhibitory alpha 2-adrenoceptors. Propranolol inhibited isoprenaline induced cAMP accumulation stereoselectively; pD2-values were 8.2 for (-)-propranolol, 5.6 for atenolol and 7.5 for ICI 118,551, suggesting a predominance of beta 2-adrenoceptors. 5. Specific 125IPIN binding to macrophage membranes was rapid and saturable. Non-specific binding was determined in the presence of 1 microM (-)-propranolol. KD values were 71 +/- 7 pM and the density of specific binding sites was 36 +/- 3 fmol mg-1 protein (three experiments on a membrane pool from 10 subjects; r values for Scatchard analyses = 0.98 +/- 0.01). Similar values were obtained when 200 microM isoprenaline (+ GTP) was used to assess non-specific binding. Competition experiments again showed stereoselectivity for propranolol and a predominance of beta 2-adrenoceptors, as judged by the displacement of specific 125IPIN binding by atenolol and ICI 118,551. 6. Macrophages from smokers responded with less marked cAMP accumulation upon stimulation with isoprenaline or PGE1 than did cells from non-smokers (difference approximately 30%; P less than 0.05 for both agonists) in the presence of IBMX. Thus macrophages from smokers may produce less cAMP due to post-receptor changes in responsiveness.(ABSTRACT TRUNCATED AT 400 WORDS)
1-Methyl-3-isobutylxanthine↗
Different cell surface and phagocytic properties in mononuclear phagocytes from blood and alveoli. A comparative study of blood monocytes and alveolar macrophages from human nonsmokers using flow cytofluorometry.
Flow cytofluorometry was used to compare blood monocytes (BMs) and alveolar macrophages (AMs) from the same nonsmoking subject (n = 13). Autofluorescence was quantified, cell surface markers (HLA-DR, CR3) were detected by monoclonal antibodies, and phagocytic ability was determined using C3b-coated yeast particles. AMs expressed more HLA-DR (p less than 0.001) and CR3 (p less than 0.01) on their surfaces than did BMs. The phagocytic capacity was enhanced in AMs compared to BMs (p less than 0.001) and the cells showed an increased autofluorescence (p less than 0.001) in the alveoli compared to blood. The findings suggest that the mononuclear phagocyte is activated when it migrates from blood to alveoli in order to adapt to the milieu in the alveolar space.
Adult↗
Effects of an inhaled corticosteroid, budesonide, on alveolar macrophage function in smokers.
Selected functions of alveolar macrophages obtained by bronchoalveolar lavage of 12 healthy smokers were examined before and after eight weeks' treatment with an inhaled glucocorticosteroid, budesonide (400 micrograms twice daily). After budesonide treatment spontaneous as well as opsonised zymosan triggered prostaglandin E2 (PGE2) secretion from harvested cells was reduced; no such reduction in opsonised zymosan triggered leukotriene B4 (LTB4) production was observed. Neither the capacity to phagocytose opsonised yeast particles nor the superoxide radical generation triggered by the calcium ionophore A23187, 4 beta-phorbol 12-myristate 13-acetate (PMA), or opsonised zymosan ex vivo were more than marginally affected by the glucocorticosteroid treatment in vivo. Lavage fluid concentrations of angiotensin converting enzyme (ACE), however, after treatment were twice those before treatment and concentrations of fibronectin were reduced to half. Albumin concentrations in lavage fluid were not affected by the glucocorticosteroid treatment. In separate experiments treatment of alveolar macrophages with 10(-7) or 10(-6) M budesonide overnight in vitro did not affect their superoxide radical or PGE2 generation but significantly blocked LTB4 release. These data indicate that inhaled gluco-corticosteroid treatment may affect synthesis or release (or both) of ACE and fibronectin by alveolar macrophages from healthy smokers whereas other functions of these cells, such as the generation of reactive oxygen derived products ex vivo, are only marginally affected.
Administration, Inhalation↗