Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antisera against isolated outer membrane (OM) proteins I and II of Escherichia coli O26 K60 were elicited in rabbits. Antisera obtained after intramuscular administration with Freund's complete adjuvant showed high titres of specific antibodies. Intravenous administration of the same preparations yielded a considerable antibody response against bacterial lipopolysaccharide, a minor contaminant of the protein preparations. Antibody titres against OM proteins I and II, lipopolysaccharide and murein-lipoprotein were determined by the enzyme-linked immunosorbent assay (ELISA) in these sera, and in antisera elicited against whole formaldehyde-fixed bacteria or isolated OM. Comparison of ELISA with single radial immunodiffusion and interfacial immunoprecipitation tests revealed that ELISA was not only the most uniformly applicable, but also the most specific and the most convenient method. In double diffusion tests no cross-reactivity between proteins I and II was seen. Antibodies against proteins I and II, lipopolysaccharide and lipoprotein could be specifically absorbed from the sera with the appropriate antigen preparations. Absorption experiments with intact E. coli O26 K60, Tris/EDTA-sheared bacteria and isolated OM revealed that antibodies against protein I were hardly absorbed at all probably because the antibody, evoked against denatured protein I, did not react with the protein in its native configuration. Antibodies against protein II and lipoprotein were absorbed by intact as well as by sheared bacteria, but to a much greater extent by isolated OM, which indicates that these OM components are accessible from the outside, but that they are situated relatively deep in the OM structure.
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PMID:Preparation and quantitative determination of antibodies against major outer mambranes proteins of Escherichia coli O26 K60. 677 43

The effect of the environmental pollutants, diesel exhaust particles (DEP) and formaldehyde (FA), on the production of pro-inflammatory cytokines (interleukin (IL)-1alpha, IL-1beta, tumor necrosis factor (TNF)-alpha and IL-8) by normal human dermal keratinocytes (hKCs) was investigated. Normal hKCs were incubated with various concentrations of DEP (0.4, 0.8, 4, or 20 microg/ml) or FA (0.25, 0.5, 1, or 5 microg/ml), and cytokine production was then determined by enzyme-linked immunosorbent assay (ELISA). DEP (20 microg/ml) induced IL-1beta production without altering cell growth. The increased production of IL-1beta induced by this concentration of DEP was further enhanced by the presence of phorbol 12-myristate 13-acetate (PMA), although PMA alone did not affect the levels of IL-1beta. IL-8 production was also increased by DEP (0.4 and 0.8 microg/ml), which is consistent with the results that these concentrations of DEP increased the number of cells significantly after 72 h incubation. Although FA alone did not stimulate the production of IL-1beta or IL-8 by keratinocytes, FA (0.5 microg/ml and 5 microg/ml) significantly increased IL-8 and IL-1beta production, respectively, in cells stimulated with PMA. IL-1alpha production was not modulated by FA or DEP even in the presence of PMA. TNF-alpha was produced by unstimulated keratinocytes at barely detectable levels after 48 h incubation. Although basal levels of TNF-alpha in the culture supernatants were increased after stimulation with PMA, neither pollutant alone nor combination with PMA affected the levels of TNF-alpha. These in vitro findings suggest that environmental pollutants may act as modulating factors of cutaneous inflammation by affecting the ability of keratinocytes to release pro-inflammatory cytokines.
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PMID:Effect of environmental pollutants on the production of pro-inflammatory cytokines by normal human dermal keratinocytes. 1009 52

Physicochemical techniques such as gamma-irradiation, membrane disruption by detergents like sodium dodecyl sulfate (SDS), and fixation with formaldehyde or paraformaldehyde are routinely used to inactivate biological specimens from patients and animals infected with Filoviruses and Arena viruses that must be studied in BSL 4 facilities. The effects of these inactivation techniques on the levels of immunologically active proteins like cytokines and chemokines are not known. Therefore, we investigated the effect of several decontamination techniques on the immunoreactivity and bioactivity of the inflammatory cytokines IL-1beta, IL-6, TNF-alpha, IL-12, and IFN-gamma, the anti-inflammatory cytokine IL-10, and the chemokine IL-8 in biological specimens. SDS (96%-100% reduction), paraformaldehyde treatment (11%-100% reduction), and heat denaturation (75%-100% reduction) were found to decrease markedly the levels of all cytokines and chemokines as measured by enzyme-linked immunosorbent assays. In contrast, gamma-irradiation was found to have little or no effect on the immunoreactivity of these cytokines/chemokines and on the biological activity of tumor necrosis factor (TNF) alpha. Our data suggest that, of the agents tested, gamma-irradiation is the preferred technique for inactivation of biological specimens containing viral agents that require the use of BSL 4 for immunological studies.
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PMID:Cytokine measurement in biological samples after physicochemical treatment for inactivation of biosafety level 4 viral agents. 1050 67

Polymorphonuclear cell (PMN) infiltration is a hallmark of ricin-induced mucosal inflammation, yet the cellular processes involved in initiating this reaction remain undefined. In this study we report that ricin stimulates the human monocyte/macrophages cell line 28SC to secrete IL-8, a potent PMN chemoattractant. IL-8 release in response to ricin was both dose- and time-dependent. 28SC cells did not secrete IL-8 when exposed to formaldehyde-inactivated holotoxin or ricin B subunit. Furthermore, IL-8 induction could be blocked by brefeldin A, which inhibits ricin translocation into the cytosol. As predicted from the literature, we observed elevated levels of p38 mitogen activated protein kinase (MAPK), a post-transcriptional regulator of IL-8, in 28SC cells as early as 3h after ricin exposure. Treatment of 28SC cells with the pyridylimidizole analogue SB203580, a known inhibitor of p38 MAPK, suppressed ricin-mediated IL-8 release. We conclude that ricin stimulates human monocyte/macrophages to produce IL-8 by activation of the p38 MAPK pathway, raising the possibility that p38 MAPK inhibitors may potentially serve as therapeutic agents to suppress mucosal inflammation associated with ricin intoxication.
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PMID:Ricin induces IL-8 secretion from human monocyte/macrophages by activating the p38 MAP kinase pathway. 1643 99

This study investigated a range of phenol-formaldehyde-aniline-based pyrolysed carbon matrices and their component materials, for their ability to adsorb a range of inflammatory cytokines crucial to the progression of sepsis. The efficiency of adsorption of the target molecules from human plasma was assessed and compared to that of Adsorba 300C, a commercially available cellulose-coated activated charcoal. Results indicate that a number of the primary carbon/resin materials demonstrate efficient adsorption of the cytokines studied here (TNF, IL-6 and IL-8), comparable to other adsorbents under clinical investigation. Our findings also illustrate that these adsorbent capabilities are retained when the primary particles are combined to form a pyrolysed carbon matrix. This capability will enable the engineering of the carbon matrix porosity allowing a blend of carbonised particle combinations to be tailored for maximum adsorption of inflammatory cytokines. The present findings support further investigation of this carbon material as a combined carbon-based filtration/adsorbent device for direct blood purification.
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PMID:The in vitro adsorption of cytokines by polymer-pyrolysed carbon. 1680 58

Chemistry of hazardous air pollutants has been studied for many years, yet little is known about how these chemicals, once reacted within urban atmospheres, affect healthy and susceptible individuals. Once released into the atmosphere, 1,3-butadiene (BD) reacts with hydroxyl radicals and ozone (created by photochemical processes), to produce many identified and unidentified products. Once this transformation has occurred, the toxic potential of atmospheric pollutants such as BD in the ambient environment is currently unclear. During this study, environmental irradiation chambers (also called smog chambers), utilizing natural sunlight, were used to create photochemical transformations of BD. The smog chamber/in vitro exposure system was designed to investigate the toxicity of chemicals before and after photochemical reactions and to investigate interactions with the urban atmosphere using representative in vitro samples. In this study, we determined the relative toxicity and inflammatory gene expression induced by coupling smog chamber atmospheres with an in vitro system to expose human respiratory epithelial cells to BD, BDs photochemical degradation products, or the equivalent ozone generated within the photochemical mixture. Exposure to the photochemically generated products of BD (primarily acrolein, acetaldehyde, formaldehyde, furan and ozone) induced significant increases in cytotoxicity, IL-8, and IL-6 gene expression compared to a synthetic mixture of primary products that was created by injecting the correct concentrations of the detected products from the irradiation experiments. Interestingly, exposure to the equivalent levels of ozone generated during the photochemical transformation of BD did not induce the same level of inflammatory cytokine release for either exposure protocol, suggesting that the effects from ozone alone do not account for the entire response in the irradiation experiments. These results indicate that BDs full photochemical product generation and interactions, rather than ozone alone, must be carefully evaluated when investigating the possible adverse health effects to BD exposures. The research presented here takes into account that photochemical transformations of hazardous air pollutants (HAPs) does generate a dynamic exposure system and therefore provides a more realistic approach to estimate the toxicity of ambient air pollutants once they are released into the atmosphere.
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PMID:Atmospheric photochemical transformations enhance 1,3-butadiene-induced inflammatory responses in human epithelial cells: The role of ozone and other photochemical degradation products. 1686 Feb 97

Acute lung injury (ALI) makes up a spectrum of disease that is commonly defined as "acute non-cardiogenic edematous lung injury". It may contribute to morbidity and mortality in the critically ill patient in the intensive care unit. ALI was induced by oleic acid in rabbits. During the experiment, blood samples were taken from cervical artery and subjected to blood-gas analysis at different time points after oleic acid injection. Shortly after the rabbits were killed at 3 hour after iv OA injection, bronchoalveolar lavage fluid (BALF) was colleted, and the concentrations of protein, platelet-activating factor (PAF), intercellular adhesion molecule-1 (ICAM-1), interleukin 8 (IL-8) in BALF were then measured by ELISA. The ratio of wet to dry weight (W/D) of left lung was calculated to assess alveolar edema. Lung tissue was fixed in formaldehyde and stained with HE, and examined under a light microscope. The OA-induced elevation of arterial blood oxygen pressure was inhibited, as well as PAF, ICAM-1, IL-8 in BALF in rupatadine group. Furthermore, rupatadine also decreased the concentration of protein in BALF and inhibited the increase of the W/D weight ratio significantly. Light microscopic findings showed that the damage in rupatadine groups was far less severe than that in OA model group. Pretreatment with rupatadine has a beneficial effect on acute lung injury induced by oleic acid in rabbits. The ultimate reduction of inflammatory factors was involved, at least in part, in the mechanism of action of rupatadine effects.
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PMID:[Protective effect of rupatadine against oleic acid-induced acute lung injury in rabbits]. 1752 Aug 22

This study presents results on soy protein isolate (SPI) biofilm production and the corresponding effect on the stability and toxicity of the derived films. SPI biofilms were prepared from SPI chemically treated with formaldehyde at various concentrations (0%, 1%, 2%, and 3%) as cross-linking agents. In vitro SPI biofilm degradation was evaluated as a function of water absorption leading to weight and size modifications. SPI biofilm toxicity was determined as a function of human keratinocyte and fibroblast adhesion, viability, and proliferation. Cytokine gene expression supported this using reverse transcriptase polymerase chain reaction techniques. Our results confirm that SPI can be used to produce biofilms. The resulting SPI biofilms without formaldehyde swell significantly, which leads to their physical instability. Formaldehyde treatment enhanced the mechanical properties of these biofilms by covalently cross-linking polypeptide chains. The decreased water absorption was dependent on the amount of formaldehyde present. SPI biofilms with 2% and 3% formaldehyde were highly stable and easier to manipulate than those with 0% and 1% formaldehyde. Tissue culture analyses revealed that the SPI biofilms without formaldehyde were non-toxic to human cells (keratinocytes and fibroblasts). The presence of formaldehyde in biofilms did not have any effects on cell viability, adhesion, or proliferation. This was supported by the high level of messenger RNA expression of interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha by the keratinocytes and of IL-6 and IL-8 by the fibroblasts. Overall, we produced a stable, non-toxic soy protein support, which may be of potential interest in medical applications such as cell culture matrices and damaged tissue replacement.
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PMID:Production and in vitro evaluation of soy protein-based biofilms as a support for human keratinocyte and fibroblast culture. 1893 36

Stimulation of CXC-type chemokine receptor 2 (CXCR2)-transfected cells by Gro-alpha or IL-8 induced (i) CXCR2 internalization, (ii) phosphorylation of ERK1/2 (pERK) and (iii) translocation of nuclear factor of activated T cells (NFAT) into the nucleus. Employing high content screening (HCS; i.e. fluorimetric imaging combined with image analysis) these three ligand-induced events were quantified by using a CXCR2-specific antibody, an antibody recognizing phosphorylated ERK1/2 (pERK) and a red fluorescent protein (RFP) in fusion to transiently overexpressed NFAT, respectively. As an RFP, we applied a recently developed mutant of an Entacmaea quadricolor fluorescent protein with favorable properties for HCS, such as high fluorescence brightness, photostability, large Stokes shift, and stability with regard to formaldehyde. Receptor internalization was closely coupled with ERK signalling both when analyzed in regard of stimulation by physiological CXCR2 ligands and when observed in the presence of antagonistic test compounds. A means of increasing the throughput or of broadening the pharmacological characterization of test compounds is the use of multiplexed imaging. Indeed, CXCR2 internalization could be multiplexed with the NFAT nuclear translocation by fixation at approximately 45 min after Gro-alpha stimulation. This multiplexing demonstrated that Gro-alpha-induced CXCR2 internalization was tightly correlated with Gro-alpha-induced NFAT translocation, also on the single cell level. The analysis of ERK phosphorylation, NFAT translocation and receptor internalization enabled the profiling of antagonistic test compounds with respect to G-protein signalling and possible receptor desensitization liabilities.
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PMID:High content screening of CXCR2-dependent signalling pathways. 2021 72

Asthma is a public health problem worldwide, and indoor air pollution considered to be a potential etiology. New tools need to be developed to study the effects of air pollutants in vitro and modelize inhalation exposure. This study was thus set up to design an in vitro model, using a direct exposure device to study the cellular effects of air pollutants at environmental doses on lung epithelial cells, and apply this to gaseous formaldehyde (FA). A549 cells were exposed using the direct exposure device (air/liquid interface) to FA without, after and before TNFalpha (1 ng/mL) sensitization. 24h after exposure, cellular viability (XTT) and inflammation (IL-6, IL-8 and MCP-1) were assessed. No effects on cellular viability were observed for concentrations < or =50 microg/m(3). After TNFalpha sensitization, FA-exposure induced a significant increase in IL-8 (p<0.001), which could lead to the initiation or pathogenesis of non-specific respiratory inflammation. The results of this study demonstrate the feasibility and sensitivity of the exposure system for testing inflammatory cellular effects of indoor gaseous compounds at environmental doses directly on human respiratory cells.
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PMID:An in vitro model to evaluate the inflammatory response after gaseous formaldehyde exposure of lung epithelial cells. 2022 36


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