Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is considerable interest in the potential health effects resulting from inhalation of acidic aerosols. However, except for well documented irritant effects and acid-induced changes in lung clearance function, other potential health effects have not been well defined. This study was designed to provide further insight regarding the relationship of sulfuric acid aerosol to the pathogenesis of respiratory disease by describing the effects of inhaled acid on the release and/or activity of biologically active mediators critical for maintaining pulmonary immunocompetence and resistance against infectious diseases. Results of this study demonstrated that a single inhalation exposure of rabbits to environmentally relevant and higher concentrations of sulfuric acid depresses the release/activity of lipopolysaccharide-stimulated tumor necrosis factor-alpha and also reduces the ability of pulmonary macrophages to produce superoxide anion radical in response to opsonised zymosan. These findings should be considered when evaluating the health risks associated with sulfuric acid exposure.
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PMID:Modulation of pulmonary immune defense mechanisms by sulfuric acid: effects on macrophage-derived tumor necrosis factor and superoxide. 133 73

Tumor necrosis factor plays a central role in the mediation of the pathophysiological sequelae of infection and inflammation in animals and humans. The elucidation of its role in respiratory disease of swine has not been investigated, due in part to the lack of a sensitive and specific quantitative assay for its presence in tissue and fluid samples. Here we describe the detection of porcine tumor necrosis factor utilizing L929 murine fibroblast cells and characterize various parameters affecting assay sensitivity. Plating cell density and length of exposure time to test supernatants were the most critical factors. Using standard assay conditions as described here, porcine tumor necrosis factor was detected in alveolar macrophage conditioned media diluted more than 400-fold. Specificity of the assay for porcine tumor necrosis factor was shown by inhibition of cytotoxicity with neutralizing polyclonal antibodies for human recombinant tumor necrosis factor. Furthermore, comparisons of bioactivity with tumor necrosis factor mRNA levels from lipopolysaccharide-stimulated porcine alveolar macrophages indicated that the L929 bioassay was specific for porcine tumor necrosis factor.
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PMID:Detection of tumor necrosis factor alpha from porcine alveolar macrophages using an L929 fibroblast bioassay. 171 31

A semi-purified outer membrane anionic antigen (AA) fraction was isolated from Haemophilus somnus by a modified procedure of anion exchange chromatography to yield a protein fraction free of lipopolysaccharides (LPS). The AA fraction (1 mg) was administered with or without the homologous lipopolysaccharide (10 micrograms/kg body weight) as vaccines to groups of cattle twice, three weeks apart. A control group which did not receive any antigen was included in the trial. Six weeks after the first vaccination, the animals were challenged intratracheally with a virulent pneumonic strain of H. somnus (70986) and observed for clinical signs of respiratory disease. The cattle were euthanized six days later and the lungs were evaluated for the severity of lesions macroscopically as well as histopathologically. Vaccination with AA alone provided the best protection against pneumonia as indicated by significantly lower clinical scores, less extensive gross lung lesions and mild histopathological lesions with immune cell infiltration. However, when AA was combined with LPS in the vaccination, this protective effect was negated and the animals showed more detrimental histopathological lesions than the controls.
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PMID:The protective effect of vaccination against experimental pneumonia in cattle with Haemophilus somnus outer membrane antigens and interference by lipopolysaccharide. 237 12

Recent studies suggest that a group of Chlamydia strains known as TWAR, which are now proposed to be a new species called Chlamydia pneumoniae, may be a frequent cause of respiratory disease in the United States and many other countries. Current serotesting methods do not allow rapid screening of large numbers of samples to distinguish C. trachomatis exposure from C. pneumoniae exposure. We developed an enzyme immunoassay to decrease cross-reactivity between immunoglobulin G antibodies reactive with C. trachomatis and C. pneumoniae. Elementary bodies of C. trachomatis or C. pneumoniae were treated with a detergent-chelating solution to decrease the reactivity of the common lipopolysaccharide antigens. Sera from four groups of patients, totaling 143 persons, were tested by this assay. The prevalences of titers of greater than or equal to 128 to C. trachomatis and C. pneumoniae, respectively, were as follows: (i) for 23 women seropositive for C. trachomatis by the microimmunofluorescence test, 21 (91%) and 18 (78%); (ii) for 50 adult blood donors, 13 (26%) and 39 (78%); (iii) for 40 sexually transmitted disease clinic patients, 20 (50%) and 32 (80%); (iv) for 30 healthy children 5 to 7 years old, 0 (0%) and 8 (27%). Western blots (immunoblots) of each antigen corroborated the differential reactivity of C. trachomatis-positive, C. pneumoniae-negative and C. trachomatis-negative, C. pneumoniae-positive serum samples. Western blots of serum samples from rabbits immunized with either C. trachomatis or C. pneumoniae elementary bodies revealed at least two protein bands (30 and 80 kilodaltons) which appeared to represent unique C. pneumoniae antigens.
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PMID:Enzyme immunoassay to determine exposure to Chlamydia pneumoniae (strain TWAR). 259 40

Serum samples obtained from feeder calves before and after entry into the market system (days 0 to 7) were assayed for antibodies to Pasteurella hamolytica biotype A, serotype 1 capsular polysaccharide (CPS) and lipopolysaccharide/outer membrane protein (LPSp) by isotype in a kinetic-augmented, antigen-capture ELISA. These test results, plus indirect hemagglutination (IHA) antibody titers, and hemolysin-in-gel test (HIGT) findings were compared with clinical performance data during the initial 4 weeks in the feedlot (receiving period). High concentrations of HIGT antibody, at the point of initial assembly of feeder calves at weaning and during the subsequent 7-day marketing period, were associated with freedom from bovine respiratory disease (BRD) during the receiving period. High or rapidly increasing concentrations of anti-CPS IgG1 during the marketing period were also associated with less BRD. However, high concentrations of anti-LPSp IgG1 during the marketing period were associated with increased BRD during the receiving period. There was no correlation between the concentrations of antibody determined by IHA tests early in the marketing period and freedom from BRD during the receiving period. High concentrations of antibody determined by this test at entry into the feedlot (day 7) were associated with a high incidence of BRD. Calves vaccinated with a P haemolytica bacterin had significantly (P less than 0.05) higher HIGT values and concentrations of anti-LPSp IgG1 and IHA antibody than did nonvaccinated calves on entry into the feedlot (day 7). Vaccination appeared to have little effect on the amount of anti-CPS IgG1. Of all the tests used to quantitate antibody, the HIGT correlated best with clinical performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antibodies to Pasteurella haemolytica somatic antigens in two models of the bovine respiratory disease complex. 271 11

We studied various means of inducing avian phagocytes to migrate to the respiratory tract. No significant and consistent increases in the number of avian respiratory phagocytes (ARP) were elicited by intravenous inoculation with Escherichia coli lipopolysaccharide (LPS), Saccharomyces cerevisiae glucan (G), and Freund's incomplete adjuvant (FIA) in a water-in-oil-in-water emulsion; subcutaneous inoculation with the LPS-G-FIA homogenate; or aerosolized exposure to LPS-G-FIA, thioglycolate, and proteose-peptone. Intravenous inoculation with heat-killed Corynebacterium parvum resulted in a significant increase in the number of ARP by day 6 after inoculation; intratracheal inoculation of C. parvum effected a more rapid and higher level of phagocyte migration to the respiratory tract. Intratracheally administered E. coli induced significant migration of phagocytes to the respiratory system so that by 24 hours postinoculation, the group average number of ARP was about 50-100 times as high as the number in unstimulated control birds. None of the birds yielding high numbers of phagocytes from their respiratory tract had signs of respiratory disease.
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PMID:Cellular defense of the avian respiratory system. Influx of phagocytes: elicitation versus activation. 344 37

Oral administration of the bacterial immunomodulator Broncho-Vaxom (OM-85), a lysate of eight bacteria strains commonly causing respiratory disease, has been shown to enhance the host defence of the respiratory tract. In this study we examined the effect of orally administered (in vivo) OM-85 on stimulus-induced cytokine and nitric oxide secretion by rat alveolar macrophages in vitro. The results show that alveolar macrophages isolated from OM-85-treated rats secreted significantly more nitric oxide, tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta upon in vitro stimulation with lipopolysaccharide (LPS), whereas, in contrast, LPS-induced IL-6 secretion was significantly lower. The observed effects of in vivo OM-85 treatment on stimulus-induced cytokine secretion in vitro are not due to a direct effect of OM-85 on the cells, because in vitro incubation of alveolar macrophages with OM-85 did not result in altered activity, nor did direct intratracheal instillation of OM-85 in the lungs of rats result in altered alveolar macrophage activity in vitro. It is hypothesized that oral administration of OM-85 leads to priming of alveolar macrophages in such a way that immune responses are non-specifically enhanced upon stimulation. The therapeutic action of OM-85 may therefore result from an enhanced clearance of infectious bacteria from the respiratory tract due to increased alveolar macrophage activity.
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PMID:Changes in cytokine and nitric oxide secretion by rat alveolar macrophages after oral administration of bacterial extracts. 764 13

Inflammatory cytokines, including interleukin (IL)-1 alpha, IL-1 beta, IL-8, and tumor necrosis factor alpha (TNF-alpha) are produced by macrophages in response to a variety of pathogenic stimuli. We show here that the expression of inflammatory cytokines is suppressed by IL-4 at the transcriptional level. Interleukin-4, when added together with bacterial lipopolysaccharide (LPS), suppressed LPS-induced increases in mRNA levels of IL-1 alpha, IL-1 beta, IL-8, and TNF-alpha in alveolar macrophages. The level of suppression was dependent on dose and time of exposure and reached a maximum of 75-80% of uninduced values for IL-1 alpha, IL-8, and TNF. Interleukin-1 beta expression was completely inhibited by IL-4. The amount of secreted protein, as determined by TNF-alpha bioassay, was also suppressed by IL-4. Half-maximal suppression occurred at IL-4 concentrations between 0.02 and 0.1 ng/ml for all inflammatory cytokines. Nuclear run-on assays showed that IL-4 suppressed transcriptional activity of all inflammatory cytokines. Messenger RNA stability was not changed by IL-4. The data suggest that IL-4 plays an important transcriptional role in the regulation of alveolar macrophage inflammatory activities in respiratory disease and raise the possibility that IL-4 may function in vivo as a coordinator of inflammatory and immune responses.
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PMID:Interleukin-4 suppresses inflammatory cytokine gene transcription in porcine macrophages. 793 Sep 48

Three viruses known to be associated with the bovine respiratory disease complex were evaluated in vitro for potential impact upon the procoagulant activity (PCA) of bovine alveolar macrophages (bAM). Cultures of bAM were inoculated with bovine parainfluenza virus Type 3 (PI-3), cytopathic bovine viral diarrhea virus (cpBVDV), non-cytopathic BVDV (ncpBVDV), or bovine herpes virus Type 1 (BHV-1) and incubated for several time periods (24, 48, 72, 96 h). BAM were then exposed to E. coli lipopolysaccharide (LPS), or LPS with bovine serum. The amount of PCA expressed was quantified using a chromogenic assay. Viral inoculation increased bAM expression of PCA (P < 0.01). The increase in PCA expression was larger at higher rates of viral inoculation (P < 0.01). LPS enhanced PCA expression by bAM at low rates of viral inoculation (P < 0.01). The effect of LPS-serum treatment was greater than the LPS alone (P < 0.01). At high rates of viral inoculation, LPS had no enhancing effect on PCA expression. The effect of LPS on virus inoculated bAM varied with virus type, rate of inoculation, and duration of virus exposure (P < 0.01). The results suggest that these four viruses initiate the production of PCA by bAM independently of LPS. In the field situation, an initial viral infection may induce fibrin deposition in the pulmonary alveoli prior to the establishment of a secondary gram negative bacterial infection.
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PMID:Induction of procoagulant activity in virus infected bovine alveolar macrophages and the effect of lipopolysaccharide. 934 37

This review provides a clear explanation of the current status of two common airborne contaminants, lipopolysaccharide and (1-->3)-beta-D-glucan, in the induction of indoor air-related disease. A full description of the origin of these two products is given together with information of their structure and function. Details of the biochemical mechanisms by which they interact with human cells and the physiological consequences of these interactions are outlined. Both compounds play a key role in the induction of airway inflammation and this paper highlights the environmental importance in the work place and home of these inhaled agents in terms of respiratory disease.
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PMID:Something in the air: endotoxins and glucans as environmental troublemakers. 950 30


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