Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophil infiltration in the synovia is an important feature of the local inflammatory process associated with rheumatoid arthritis. The present study is focused on the effects exerted in vitro by the synovial fluid versus serum on the respiratory burst of granulocytes isolated either from blood or synovial fluid of rheumatoid arthritis patients. The respiratory burst was evaluated as superoxide anion release, by lucigenin-amplified chemiluminescence. Our data show that the respiratory burst of granulocytes isolated from rheumatoid arthritis patients might trigger a significant oxidative stress both in periphery and the inflamed joint. These cells show no pathological pattern when activated in vitro by the chemotactic peptide fMLP, heterologous synovial fluid or serum. Acellular synovial fluid amplifies the superoxide anion release induced by fMLP more than the corresponding serum, indicating that a bacterial infection in the joint might enhance the oxidative damage in the inflamed synovium.
J Cell Mol Med
PMID:Effects of synovial fluid on the respiratory burst of granulocytes in rheumatoid arthritis. 1206 1

Most cystic fibrosis (CF) patients die of lung failure, due to the combined effects of bacterial infection, neutrophil-mediated inflammation, and airway obstruction by hyperviscous mucus. To this day, it remains unclear where and how this pathological vicious circle is initiated in vivo. In particular, it has proven difficult to investigate whether inflammatory pathways are dysregulated in CF airways independently of infection. Also, the relative involvement of large (tracheobronchial) vs. small (bronchiolar) airways in CF pathophysiology is still unclear. To help address these issues, we used an in vivo model based on the maturation of human fetal CF and non-CF small airways in severe combined immunodeficiency mice. We show that uninfected mature CF small airway grafts, but not matched non-CF controls, undergo time-dependent neutrophil-mediated inflammation, leading to progressive lung tissue destruction. This model of mature human small airways provides the first clear-cut evidence that, in CF, inflammation may arise at least partly from a primary defect in the regulation of neutrophil recruitment, independently of infection.
Am J Physiol Lung Cell Mol Physiol 2002 Aug
PMID:Primary inflammation in human cystic fibrosis small airways. 1211 7

From the many peptide families that are induced upon bacterial infection and can be isolated from all classes of animals, the short, proline-rich antibacterial peptides enjoy particular interest. These molecules were shown to inactivate an intracellular biopolymer in bacteria without destroying or remaining attached to the bacterial cell membrane, and as such emerged as viable candidates for the treatment of mammalian infections. These peptides were originally isolated from insects, they kill mostly gram-negative bacteria with high efficiency and they show structural similarities with longer insect- and mammal-derived antimicrobial peptides. However, while the distant relatives appear to carry multiple functional domains, apidaecin, drosocin, formaecin and pyrrhocoricin consist of only minimal determinants needed to penetrate across the cell membrane and bind to the target biopolymer. These peptides appear to inhibit metabolic processes, such as protein synthesis or chaperone-assisted protein folding. Pyrrhocoricin derivatives protect mice from experimental infections in vivo, suggesting the utility of modified analogs in the clinical setting. Sequence variations of the target protein at the peptide-binding site may allow the development of new peptide variants that kill currently unresponsive strains or species.
Cell Mol Life Sci 2002 Jul
PMID:The short proline-rich antibacterial peptide family. 1222 61

Four genes encoding small proteins with significantly high glycine content have been identified from root nodules of Medicago sativa. All of these proteins as well as their Medicago truncatula homologues carried an amino terminal signal peptide and a glycine-rich carboxy terminal domain. All except nodGRP3 lacked the characteristic repeat structure described for cell wall and stress response-related glycine-rich proteins (GRP). Expression of these GRP genes was undetectable in flower, leaf, stem, and hypocotyl cells, whereas expression was highly induced during root nodule development, suggesting that GRP genes act as nodulins. Moreover, none of these nodule-expressed GRP genes were activated by hormones or stress treatments, which are inducers of many other GRPs. In Rhizobium-free spontaneous nodules and in nodules induced by a noninfective mutant strain of Sinorhizobium meliloti, all these genes were repressed, while they were induced in Fix- nodules, unaffected in bacterial infection, but halted in bacteroid differentiation. These results demonstrated that bacterial infection but not bacteroid differentiation is required for the induction of the nodule-specific GRP genes. Differences in kinetics and localization of gene activation as well as in the primary structure of proteins suggest nonredundant roles for these GRPs in nodule organogenesis.
Mol Plant Microbe Interact 2002 Sep
PMID:Glycine-rich proteins encoded by a nodule-specific gene family are implicated in different stages of symbiotic nodule development in Medicago spp. 1223 98

Collagenous and eosinophilic colitis are rare diseases characterised by chronic watery diarrhoea. Radiographic evaluation of the gastrointestinal tract and colonoscopy are usually non-diagnostic since as many as one-third of patients will have minor abnormalities. To date a few investigators have reported increased fluorine-18 fluorodeoxyglucose ((18)F-FDG) uptake on positron emission tomography (PET) in patients with acute enterocolitis, but there have been no reports on the use of (18)F-FDG PET for the diagnosis of collagenous or eosinophilic colitis in an early clinical stage. The aim of this preliminary study was to evaluate the usefulness of (18)F-FDG PET in the early diagnosis of patients with colitis. We investigated five women (mean age 61.2+/-12.1 years) who had been diagnosed as having colitis in an early clinical stage. In all but one of the patients, the diagnosis of colitis was based on biopsy. Magnetic resonance colonography, ultrasonography and colonoscopy were performed in all but one of the patients. Two women were identified as having collagenous colitis in an early clinical stage. Another two patients had eosinophilic colitis. The morphological imaging methods, magnetic resonance colonography and ultrasonography, yielded no suspicious findings, and the results of colonoscopy similarly showed no abnormalities. One patient had colitis due to bacterial infection. In all patients (18)F-FDG PET showed a pathological increase in tracer uptake in the large bowel, suggestive of colitis. In four of the five patients, colitis was confirmed by histology, and in one, by bacterial analysis. (18)F-FDG PET was able to detect colitis in an early clinical stage, when morphological imaging methods and colonoscopy were non-diagnostic. The early performance of (18)F-FDG PET imaging in patients with possible colitis is encouraging.
Eur J Nucl Med Mol Imaging 2002 Oct
PMID:(18)F-FDG positron emission tomography in the early diagnosis of enterocolitis: preliminary results. 1227 24

The objective of this study was to document the reduced acute phase response that appears in children with viral as opposed to bacterial infections. The white blood cell count (WBCC), the erythrocyte sedimentation rate (ESR), and leukocyte and erythrocyte adhesiveness/aggregation were determined in 36 children with acute bacterial infection, 29 children with viral infection, and 19 controls. A significant reduced WBCC, ESR, and leukocyte and erythrocyte adhesiveness/aggregation was noted in the children with acute viral infection as opposed to those with bacterial infection: 10,800 +/- 3600 and 20,000 +/- 10,000 cells/cm2, 29 +/- 21 and 53 +/- 35 mm Hg, 23 +/- 9 and 41 +/- 15%, and 3.4 +/- 5.1 and 9.8 +/- 13.6 microns, respectively. The results indicate that a reduced acute phase response can be observed in children with an acute viral infection. This can have diagnostic implications and pathophysiological consequences in terms of less flow impairment in the microcirculation due to less red and white blood cell aggregation.
Pediatr Pathol Mol Med
PMID:Reduced acute phase response to differentiate between viral and bacterial infections in children. 1253 73

Pepper ascorbate peroxidase-like (CAPOA1), thioredoxin peroxidase-like (CAPOT1), and peroxidase-like (CAPO1) clones were isolated from pepper leaves inoculated with avirulent strain Bv5-4a of Xanthomonas campestris pv. vesicatoria. CAPOA1, CAPOT1, and CAPO1 mRNA disappeared 18 to 30 h after the bacterial infection when the hypersensitive response (HR) was visible. In contrast, peroxidase activity reached a peak at 18 h after infection and then declined at 24 and 30 h when H2O2 accumulation level was maximal. These results suggest that the striking accumulation of H2O2 and strong decrease in peroxidase activity during the programmed cell death may be due to the strong suppression of CAPOA1, CAPOT1, and CAPO1 gene expression. Infection by Phytophthora capsici or Colletotricum gloeosporioides also induced the expression of the three putative peroxidase genes in pepper tissues. CAPOA1 mRNAs were in situ localized in phloem areas of vascular bundles in pepper tissues infected by Colletotricum. coccodes, P. capsici, or C. gloeosporioides. Exogenous treatment with H2O2 strongly induced the CAPOA1 and CAPOT1 transcription 1 h after treatment, while the CAPO1 transcripts accumulated 12 h after H2O2 treatment. We suggest that pepper ascorbate peroxidase and thioredoxin peroxidase genes may function as regulators of H2O2 level and total peroxidase activity in the oxidative burst during the HR to incompatible pathogen interaction in pepper plant.
Mol Plant Microbe Interact 2003 Mar
PMID:Expression of peroxidase-like genes, H2O2 production, and peroxidase activity during the hypersensitive response to Xanthomonas campestris pv. vesicatoria in Capsicum annuum. 1265 Apr 51

Pseudomonas aeruginosa is a gram-negative bacterium that causes both acute and chronic lung disease in susceptible patient populations. P. aeruginosa secretes numerous proteins and secondary metabolites, many of which have biological effects that likely contribute to disease pathogenesis. An unidentified small-molecular-weight factor was previously reported to increase IL-8 release both in vitro and in vivo. To identify this factor, we subjected the <3-kDa fraction from P. aeruginosa-conditioned medium to HPLC analysis. A peak fraction that stimulated IL-8 release was found by mass spectrometry to have a molecular mass (MM) of 224 Da. On the basis of this MM and other biochemical properties, we hypothesized that the factor was phenazine-1-carboxylic acid (PCA). Subsequent studies and comparison with purified PCA confirmed this hypothesis. Purified PCA exhibited a number of biological effects in human airway epithelial cells, including increasing IL-8 release and ICAM-1 expression, as well as decreasing RANTES and monocyte chemoattractant protein-1 (MCP-1) release. PCA also increased intracellular oxidant formation as measured by electron paramagnetic resonance and by an intracellular oxidant-sensitive probe. Antioxidants inhibited PCA-dependent increases in IL-8 and ICAM-1, suggesting that oxidants contributed to these effects. However, in contrast to the related phenazine compound pyocyanin, PCA did not oxidize NAD(P)H at physiologically relevant pH, providing preliminary evidence that PCA and pyocyanin may have distinct redox chemistries within the cell. Thus PCA is a biologically active factor secreted by P. aeruginosa that has several activities that could alter the host immune and inflammatory response and thereby contribute to bacterial disease pathogenesis.
Am J Physiol Lung Cell Mol Physiol 2003 Sep
PMID:Phenazine-1-carboxylic acid, a secondary metabolite of Pseudomonas aeruginosa, alters expression of immunomodulatory proteins by human airway epithelial cells. 1276 78

Complement is necessary for defense against lung infection with Pseudomonas aeruginosa in mice. We studied in vitro interactions between complement and P. aeruginosa and in vivo effects of complement depletion to better understand this relationship. In vitro, P. aeruginosa strain UI-18 was resistant to killing by mouse serum. However, C3 opsonized the organism (via the alternative and mannose binding lectin [MBL] pathways), and C5 convertase activity on the bacterial surface was demonstrated. In vivo, compared with normal mice, complement-deficient mice experienced higher mortality and failed to sterilize their bronchoalveolar space within 24 h of inoculation. These changes did not seem to be a result of decreased inflammation because complement-deficient mice had normal neutrophil recruitment, greater lung myeloperoxidase content, and, by 24 h, a 35-fold higher level of the CXC chemokine KC. Lung static pressure-volume curves were abnormal in infected animals but were significantly more so in complement deficient mice. These data indicate that although P. aeruginosa is resistant to serum killing, C3 opsonization and C5 convertase assembly occur on its surface. This interaction in vivo plays a central role in host survival beyond just recruitment and activation of phagocytes and may serve to limit the inflammatory response to and tissue injury resulting from bacterial infection.
Am J Respir Cell Mol Biol 2003 Oct
PMID:Murine complement interactions with Pseudomonas aeruginosa and their consequences during pneumonia. 1450 Feb 54

The change in gene expression patterns in response to host environments is a prerequisite for bacterial infection. Bacterial diseases often occur as an outcome of the complex interactions between pathogens and the host. The indigenous, usually non-pathogenic microflora is a ubiquitous constituent of the host. In order to understand the interactions between pathogens and the resident microflora and how they affect the gene expression patterns of the pathogens and contribute to bacterial diseases, the interactions between pathogenic Pseudomonas aeruginosa and avirulent oropharyngeal flora (OF) strains isolated from sputum samples of cystic fibrosis (CF) patients were investigated. Animal experiments using a rat lung infection model indicate that the presence of OF bacteria enhanced lung damage caused by P. aeruginosa. Genome-wide transcriptional analysis with a lux reporter-based promoter library demonstrated that approximately 4% of genes in the genome responded to the presence of OF strains using an in vitro system. Characterization of a subset of the regulated genes indicates that they fall into seven functional classes, and large portions of the upregulated genes are genes important for P. aeruginosa pathogenesis. Autoinducer-2 (AI-2)-mediated quorum sensing, a proposed interspecies signalling system, accounted for some, but not all, of the gene regulation. A substantial amount of AI-2 was detected directly in sputum samples from CF patients and in cultures of most non-pseudomonad bacteria isolated from the sputa. Transcriptional profiling of a set of defined P. aeruginosa virulence factor promoters revealed that OF and exogenous AI-2 could upregulate overlapping subsets of these genes. These results suggest important contributions of the host microflora to P. aeruginosa infection by modulating gene expression via interspecies communications.
Mol Microbiol 2003 Dec
PMID:Modulation of Pseudomonas aeruginosa gene expression by host microflora through interspecies communication. 1465 32


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