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At least 145 records · Page 8Linked to original sources
PubMed1987

[Air-borne dust and its protein in laboratory animal facilities].

Atopic individuals who were exposed to dust in animal rooms for a long time were more likely than non-atopics to have animal-related symptoms. Standard skin prick tests were performed using crude antigens from dander and urine, and 75 to 100% of atopic persons had positive skin reactions. It seems that allergens in animal rooms result from air-borne dust and the dust originates in animal urine and dander. The protein content occurs as dust particles both below and above 10 micron in diameter. The dust particles above 10 micron cannot pass through face masks, so half of the dust protein is arrested under the mask, but smaller particles pass through. In order to minimize the symptoms, we need to improve the design of cages, animal rooms, experimental rooms, ventilation systems and other protective equipment.

Adult↗
PubMed2002

Transcriptional stimulation of the surfactant protein B gene by STAT3 in respiratory epithelial cells.

The function of the lung is dependent upon differentiation and proliferation of respiratory epithelial cells and the synthesis/secretion of surfactant lipids and proteins into air space. During the respiratory inflammatory response, cytokines produced by macrophages and epithelial cells in the respiratory system have significant influence on surfactant protein homeostasis. We report here that among family members of Janus family tyrosine kinase (JAK) and signal transducers and activators of transcription (STAT), only JAK 1 and STAT3 stimulated the -500 to +41 promoter activity of the surfactant protein B (SP-B) gene in respiratory epithelial cells. JAK1 and STAT3 were co-localized in alveolar type II epithelial cells where SP-B is synthesized and secreted. Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells.

Apoproteins↗
PubMed2004

Autoimmune polyglandular syndrome type 1 and the autoimmune regulator.

The autoimmune polyglandular syndrome type I (APSI) is an auto-somal recessive disorder that is characterized by chronic mucocutaneous candidiasis, multiple autoimmune endocrinopathies, and ectodermal dystrophies. The gene that is responsible for APSI has been identified as autoimmune regulator (AIRE). More than 50 different mutations have been discovered in patients who have APSI and the defects include nonsense and missense mutations, small insertions and deletions that lead to frameshift, and splice site mutations. The 545-amino acid protein that is encoded by AIRE contains several structural motifs that are suggestive of a transcriptional regulator. We provide an overview of the clinical and genetic features ofAPSI as well as the structure and functions of the AIRE protein.

Humans↗
PubMed1999

Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air.

Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of particulate air pollution (particulate matter with an aerodynamic diameter < 10 microm, PM10 and <2.5 microm, PM2. 5). Lung injury and an imbalance of inflammatory mediators are proposed causative mechanisms, while the toxic constituents may be acidity, transition metals, organic, and biogenic materials. To compare the ability of inhalable fine particles (PM2.5), and coarse particles (PM10-2.5) to cause cell injury and cytokine production in monocytes, dichotomous Andersen samplers were used to collect size-fractionated PM10 for in vitro testing of the particle extracts. Particles from both outdoor and indoor air were collected onto Teflon filters, on nine separate occasions. Each filter was water extracted and each extract assessed for ability to cause cell death, as well as interleukin (IL)-6 and IL-8 production in human monocytes. Significant toxicity and cytokine production was induced by outdoor PM10-2.5, but not by outdoor PM2.5 or the particles collected indoors. Outdoor PM10-2.5 induced 20 times the amounts of IL-6 and IL-8 than the fine particles. Cytotoxicity was inhibited by deferoxamine, a chelator of transition metals, while cytokine production was not. On the other hand, lipopolysaccharide binding protein (LBP) completely inhibited cytokine induction by PM10-2.5, suggesting that gram-negative bacteria and/or endotoxins are components of PM10-2.5. The effective proinflammatory effects of endotoxin on macrophages may upset lung homeostasis while metals-induced cytotoxicity/necrosis may set up inflammation independent of macrophage-derived cytokines.

Acute-Phase Proteins↗
PubMed1998

Aggregation of HSA, IgG, and Fibrinogen on Methylated Silicon Surfaces.

Ellipsometry was used to quantify adsorption and tapping mode atomic force microscopy to study surface aggregation of human serum albumin (HSA), immunoglobulin G (IgG), and fibrinogen (Fib) adsorbed from aqueous solutions onto methylated silicon surfaces. After exposure to air the protein monolayers were spontaneously restructured, exposing disorganized areas with heterogeneity depending on the degree of surface methylation. The aggregation patterns also depended on some properties of the adsorbed protein (such as the number of contact points with the surface), but seemed to be almost independent of the adsorption time. The results indicate that aggregates were formed due to lateral reorganization on the adsorbed layer at the air-liquid interface during the drying process. The interpretation is that the heterogeneous structures result from a thermodynamically driven interaction between the hydrophobic surface and the similarly hydrophobic air. The main conclusion that can be extracted from this work is that fibrinogen (hydrophobic and large protein) interacts more irreversibly with the silicon surfaces than IgG, and much more so than HSA, which is less hydrophobic and smaller than fibrinogen. Copyright 1998 Academic Press.

Journal Article↗
PubMed2003

Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain.

Carbon monoxide (CO) toxicity is the result of a combination of tissue hypoxia and direct CO-mediated damage at a cellular level, since not all the signs and symptoms presented can be explained only by the formation of carboxyhaemoglobin. Mitochondria, specially the electron transport chain, seem to be the target for CO at a subcellular level. However, the direct effect of CO in individual complexes of the human mitochondrial respiratory chain has not been completely elucidated. We here studied the in vitro effect of CO on individual complexes of the mitochondrial respiratory chain of human mitochondria. We obtained muscle tissue from 10 healthy people who underwent orthopaedic surgery for hip replacement. Isolated mitochondria were incubated for 5 min. under CO concentrations of 50, 100 and 500 ppm. Afterwards, enzymatic activities of individual complexes of the mitochondrial respiratory chain were assessed in vitro and compared with those obtained in basal (synthetic air without CO) conditions. Cytochrome c oxidase (complex IV of the mitochondrial respiratory chain) activity showed a decrease from 836+/-439 nmol/min./mg of mitochondrial protein after air incubation to 670+/-401, 483+/-182, and 379+/-131 nmol/min./mg after 50, 100 and 500 ppm of CO incubation, respectively (20%, 42% and 55% decrease in cytochrome c oxidase activity). This gradual decrease in cytochrome c oxidase was found to be statistically significant (P<0.001). Other complex activities showed no any significant variation. Carbon monoxide is toxic for mitochondria in man, altering the mitochondrial respiratory chain at the cytochrome c oxidase level. This inhibition in cytochrome c oxidase may play a role in the development of the symptoms observed in acute CO poisoning, and in some diseases related to smoking.

Carbon Monoxide Poisoning↗
PubMed2004

Modification of beta-lactoglobulin by oligofructose: impact on protein adsorption at the air-water interface.

Maillard products of beta-lactoglobulin (betaLg) and fructose oligosaccharide (FOS) were obtained in different degrees of modification depending on incubation time and pH. By use of a variety of biochemical and spectroscopic tools, it was demonstrated that the modification at limited degrees does not significantly affect the secondary, tertiary, and quaternary structure of betaLg. The consequence of the modification on the thermodynamics of the protein was studied using differential scanning calorimetry, circular dichroism, and by monitoring the fluorescence intensity of protein samples with different concentrations of guanidine-HCl. The modification leads to lowering of the denaturation temperature by 5 degrees C and a reduction of the free energy of stabilization of about 30%. Ellipsometry and drop tensiometry demonstrated that upon adsorption to air-water interfaces in equilibrium modified betaLg exerts a lower surface pressure than native betaLg (16 versus 22 mN/m). Moreover, the surface elastic modulus increased with increasing surface pressure but reached significantly smaller values in the case of FOS-betaLg. Compared to native betaLg, modification of the protein with oligofructose moieties results in higher surface loads and thicker surface layers. The consequences of these altered surface rheological properties are discussed in view of the functional behavior in technological applications.

Adsorption↗
PubMed2003

Protein oxidation at the air-lung interface.

Whilst performing its normal functions the lung is required to deal with a range of toxic insults. Whether these are infectious agents, allergens or air pollutants they subject the lung to a range of direct and indirect oxidative stresses. In many instances these challenges lead to oxidative alterations of peptides and proteins within the lung. Measurement of protein oxidation products permits the degree of oxidative stress to be assessed and indicates that endogenous antioxidant defences are overwhelmed. The range of protein oxidation products observed is diverse and the nature and extent of specific oxidation products may inform us about the nature of the damaging ROS and NOS. Recently, there has been a significant shift away from the measurement of these oxidation products simply to establish the presence of oxidative stress, to a focus on identifying specific proteins sensitive to oxidation and establishing the functional consequences of these modifications. In addition the identification of specific enzyme systems to repair these oxidative modifications has lead to the belief that protein function may be regulated through these oxidation reactions. In this review we focus primarily on the soluble protein components of within the surface liquid layer in the lung and the consequence of their undue oxidation.

Animals↗
PubMed1990

Effect of nitrogenous air pollutants on changes in protein spectra with the onset of winter in the leaves and shoots of the bilberry (Vaccinium myrtillus L.).

Electrophoretic profiles of 0.1 m Tris-HCl (pH 9.0)-soluble proteins in the leaves and stems of the bilberry (Vaccinium myrtillus L.) were investigated in the latter part of the growing season (July-October), in a highly-polluted industrial area with serious forest damage (main emissions NO(2), SO(2), NH(3), urea and fertilizer dust) in Oulu, northern Finland, and in an unpolluted control forest with the same climatic and edaphic conditions. About ten protein components in the leaves and seven in the stems increased in concentration in SDS-PAGE towards the autumn, while one to four other components decreased in concentration. The pollutants in the industrial area caused a considerable decrease in the concentrations of soluble proteins, particularly in the leaves in August and September. A decrease was obtained in six components in the leaves and three components in the stems, while increases were observed in one component in the leaves (10 kDa) and four components in the stems (10, 43, 50 and 65 kDa). One reason for the lowered cold-resistance in the bilberry caused by air pollutants could thus be the lowered concentrations of certain soluble cytoplasmic proteins that protect the plant against winter conditions.

Journal Article↗
PubMed2001

Heat transfer properties, moisture loss, product yield, and soluble proteins in chicken breast patties during air convection cooking.

Chicken breast patties were processed in an air convection oven at air temperatures of 149 to 218 C, air velocities of 7.1 to 12.7 m3/min, and air relative humidities of 40 to 95%. The air humidity was controlled via introducing steam into the oven. The patties were processed to a final center temperature of 50 to 80 C. Heat flux, heat transfer coefficient, moisture loss in the cooked chicken patties, the product yield, and the changes of soluble proteins in the product were evaluated for the cooking system. During cooking, heat flux varied with the processing time. Heat flux increased with increasing air humidity. The effective heat transfer coefficient was obtained for different cooking conditions. Air humidity in the oven affected the heat transfer coefficient. The moisture loss in the cooked products increased with increasing the final product temperature and the oven air temperature. The soluble proteins in the cooked patties decreased with increasing the final product temperature. Increasing humidity increased heat transfer coefficient and therefore reduced cooking time. Reducing oven temperature, reducing internal temperature, and increasing air humidity increased the product yield. Soluble proteins might be used as an indicator for the degree of cooking. The results from this study are important for evaluating commercial thermal processes and improving product yields.

Animals↗
PubMed1999

Alteration of epithelial integrity, alkaline phosphatase activity, and fibronectin expression in lungs of rats exposed to ozone.

The deleterious effects of ozone (O3), an oxidant air pollutant, in the lung are dependent on dose and exposure duration and generally evolve with time postexposure. This study characterized the time sequence of epithelial injury and fibronectin expression in the lungs of rats exposed to O3. Bronchoalveolar lavage (BAL) fluid was analyzed for alkaline phosphatase and total protein as markers of epithelial injury and increased permeability, and fibronectin for its role in inflammation and lung injury. The results revealed a time-related increase in total protein in the BAL fluid following a 3-h exposure of rats to 1 ppm O3. The increased protein concentrations peaked at 12 h and then declined, but remained significantly higher than control at 24 h postexposure. A similar time-related significant increase also occurred for BAL fibronectin and alkaline phosphatase activity. However, the return of alkaline phosphatase levels to baseline prior to a comparable reduction in protein levels suggests repair of injured cells, but a delay in the formation of epithelial junctions that limit the transfer of serum proteins to air spaces. By cytochemistry, alkaline phosphatase activity was detected in association with lung type II epithelial cells and in BAL polymorphonuclear leukocytes (PMNs), but not in macrophages. While a significant increase in cytochemically detectable alkaline phosphatase resulted from the increase in PMN number following O3 exposure, mononuclear cells constituted the primary cell type responsible for fibronectin mRNA upregulation. While the cytochemical observations support the role of inflammatory cells in the injury process, the comparability of temporal changes in BAL protein, fibronectin, and alkaline phosphatase suggests a mechanistic role for fibronectin in lung injury.

Air Pollutants↗
PubMed2005

Genetic insights into disease mechanisms of autoimmunity.

Educating the immune system to distinguish between self and non-self is critical to ensure that an immune response is mounted against foreign antigens and not against self. A breakdown in these mechanisms can lead to the onset of autoimmune disease. Clinical and molecular data suggest that shared immunogenetic mechanisms lead to the autoimmune process. The most studied genes and molecules are the human leukocyte antigen (HLA) region and the cytotoxic T-lymphocyte-associated 4 molecule (CTLA-4). Recently progress has been achieved in narrowing down the primary variants within both gene regions, but further work is needed to determine the function and extent of the aetiological variant(s) present. Recent exciting results also suggest a role for the newly discovered lymphoid-specific phosphatase (LYP) protein. As well as these general mechanisms, disease-specific mechanisms are beginning to be elucidated, for example the role of autoimmune regulatory element 1 (AIRE1) in autoimmune polyendocrinopathy-candidiasis ectodermal dystrophy (APECED). Taken together, these data suggest that both general and disease-specific mechanisms lead to the clinical outcome of autoimmune disease and that increased understanding of these mechanisms will improve our knowledge of how autoimmune disease occurs, eventually leading to the development of novel therapeutic agents.

Antigens, CD↗
PubMed1985

Effects of protein deficiency and food restriction on lung ascorbic acid and glutathione in rats exposed to ozone.

Weanling (52 +/- 4 g) or adult (259 +/- 16 g) male Sprague-Dawley rats were fed ad libitum casein-based diets containing 4 or 16% protein. A third group (food restricted) was fed daily the 16% protein diet, but at the food intake level of the 4% protein group. After 3 wk (weanling) or 5 wk (adults), half of the rats in each group were continuously exposed to 0.64 ppm ozone for 7 d. Ascorbic acid and reduced glutathione levels were then measured. In the heart and liver from weanling rats, ascorbic acid concentrations were lower in the protein-deficient group than in either control group. In the liver from weanling rats glutathione concentrations were also reduced in response to protein deficiency. Exposure to ozone produced no additional response. For adult rats the response for liver glutathione was similar to that of the weanlings. The liver ascorbate concentration, however, was consistently lower in adult rats compared to weanlings exposed to ozone. In lungs from adult rats, the ascorbic acid concentration was lower in the protein-deficient group than in either control group. On a whole-organ basis, both ascorbic acid and glutathione were usually higher in lungs from rats exposed to ozone than from those exposed to air. Interestingly, protein deficiency did not appear to compromise the lung's ability to maintain, in relative terms, the ascorbic acid or glutathione concentration in response to ozone.

Aging↗
PubMed2002

Ethene and other biomarkers of oxidative stress in hypertensive disorders of pregnancy.

OBJECTIVE: An increase in reactive oxygen species (ROS) and lipid peroxides and a comprised antioxidant status has been implicated in the pathophysiology of severe preeclampsia. This study investigates whether oxidative stress and impaired antioxidant systems also contribute to milder forms of hypertensive disorders in pregnancy. Furthermore, ethene in exhaled air, a noninvasive measure for oxidative stress, was evaluated and compared with two other more established biomarkers. METHODS: Ethene in exhaled air, plasma protein carbonyls, and the ratio of free glutathione/oxidized glutathione (GSHfree/GSHox) as markers for oxidative stress as well as the antioxidants vitamins C and E, uric acid, glutathione, and the oxygen radical absorbance capacity (ORAC) in plasma were measured in 30 healthy nonpregnant, 14 normal pregnant, 9 women with pregnancy-induced hypertension (PIH), and 14 preeclamptic women. Pregnant participants were measured during pregnancy and after delivery. RESULTS: Women suffering from PIH and preeclampsia showed higher levels of the antioxidants vitamin E and uric acid, and lower levels of vitamin C compared with normal pregnant and nonpregnant women. All markers for oxidative stress were comparable between groups. Ethene levels showed a positive correlation with protein carbonyls but no correlation could be demonstrated with the free glutathione/oxidised glutathione ratio. CONCLUSIONS: PIH and preeclampsia are associated with minor alterations in antioxidant levels without signs of oxidative stress. Detection of ethene in exhaled air seems a promising noninvasive method to study lipid peroxidation but further research in more severe preeclampsia is needed.

Antioxidants↗
PubMed2005

Autoimmune polyendocrinopathy syndrome type 1 (APS1) and AIRE gene: new views on molecular basis of autoimmunity.

Autoimmune polyendocrinopathy syndrome type 1 (APS1) is a monogenic autoimmune syndrome, which is caused by defect in AIRE gene on chromosome 21. Several autoimmune diseases occur in APS1 patients, often starting in first two decades of life. A gene defective in APS1, autoimmune regulator (AIRE), encodes nuclear protein involved in transcriptional processes. Recent findings in animal models indicate a critical role for AIRE in regulation of self-antigen expression in thymus. Identification of the AIRE gene, detailed characterization of molecular pathogenesis of human APS1 as well as analyses of mouse models carrying targeted interruption of Aire gene have provided new views on our understanding of molecular background of autoimmunity.

Animals↗