UMLS:C0032285 - FACTA Search

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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The substrate specificity of the enzyme endo-alpha-N-acetyl-D-galactosaminidase from Diplococcus pneumonia was re-examined using bovine submaxillary mucin and remodelled antifreeze glycoprotein as substrates. Incubation with desialylated bovine submaxillary mucin, which contains six O-linked core types, indicated that the disaccharide Gal beta1-3GalNAc, which is present in very small amount, was the only glycan released, while the disaccharide GlcNAc beta1-3GalNAc, which is the major structure present, and other disaccharides, were not released. To test whether the core disaccharide Gal beta1-3GalNAc with sialic acid linked alpha2-3 to the Gal or linked alpha2-6 to the GalNAc was released, the enzyme was incubated with remodelled antifreeze glycoprotein containing (1) [3H]NeuAc alpha2-3Gal beta1-3GalNAc and (2) Gal beta1-3[[14C]NeuAc alpha2-6]GalNAc as substrates. No NeuAc-containing trisaccharide was released. These results serve to clarify the doubts of many researchers regarding the activity of this enzyme on some newly-described core types and on sialylated substrates.
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PMID:The substrate specificity of the enzyme endo-alpha-N-acetyl-D-galactosaminidase from Diplococcus pneumonia. 911 Nov 35

In rheumatoid arthritis (RA), interstitial-pneumonitis is one of the major extraarticular complications that worsens a patient's prognosis. KL-6, a human MUC1 mucin, has been reported to be a sensitive serum marker for activity of interstitial pneumonitis. We investigated the clinical significance of serum KL-6 level in patients with RA. Serum levels of KL-6 and RA-associated inflammatory markers were evaluated in 177 RA patients. The diagnosis of active interstitial pneumonitis was made by clinical symptoms, pulmonary function tests, chest X-ray film, and high resolution CT. Serum KL-6 was increased in 8 of 9 (88.9%) RA patients with active interstitial pneumonitis but in only 1 of 168 (0.6%) RA patients without active interstitial pneumonitis. No significant correlation was found between KL-6 level and conventional clinical parameters. In RA, abnormal elevation of serum KL-6 strongly indicates the complication of active interstitial pneumonitis.
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PMID:Detection of interstitial pneumonitis in patients with rheumatoid arthritis by measuring circulating levels of KL-6, a human MUC1 mucin. 933 Feb 47

KL-6, a MUC1 mucin preferentially expressed in regenerating type 2 pneumocytes, has been reported to be a sensitive serum marker for evaluating the disease activity of interstitial pneumonitis (IP). Type III procollagen N-terminal peptide (PIIIP) and type IV collagen 7S (7S collagen) have also been reported to be useful in the serological evaluation of the activity. Their levels were measured and their serodiagnostic values were compared simultaneously in patients with IP and alveolar pneumonia. The study population was 45 patients with IP and 12 patients with alveolar pneumonia. Serum KL-6 levels were measured by a specific enzyme immunoassay, and both serum PIIIP and 7S collagen concentrations by their correspondent radioimmunoassay kits. There were no significant difference of serum C-reactive protein level, which was evaluated as an indicator of inflammatory process, between IP and alveolar pneumonia patients. In IP, the abnormally elevated rate of KL-6 [80% (36/45)] was significantly higher than those of PIIIP [40% (18/45)] and 7S collagen [40% (18/45)]. In alveolar pneumonia, the rate of KL-6 [0% (0/12)] was significantly lower than those of PIIIP [33% (4/12)] and 7S collagen [25% (3/12)]. There were no significant correlations among serum levels of the markers. These observations indicate that the serodiagnostic value of KL-6 for IP is superior to that of PIIIP and 7S collagen, and that KL-6 has a characteristic to discriminate IP from alveolar pneumonia.
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PMID:Comparative studies of circulating KL-6, type III procollagen N-terminal peptide and type IV collagen 7S in patients with interstitial pneumonitis and alveolar pneumonia. 941 57

Pseudomonas aeruginosa strains are opportunistic pathogens associated with infections in immunocompromised hosts and patients with cystic fibrosis. Like many other mucosal pathogens, P. aeruginosa cells express flagella which provide motility and chemotaxis toward preferred substrates but also provide a ligand for clearance by phagocytic cells. We tested the role of flagella in the initial stages of respiratory tract infection by comparing the virulence of fliC mutants in a neonatal mouse model of pneumonia. In the absence of fliC, there was no mortality, compared with 30% mortality attributed to the parental strain PAK or 15% mortality associated with infection due to a pilA mutant PAK/NP (P < 0.0001). The fliC mutants caused pneumonia in only 25% of the mice inoculated, regardless of whether there was expression of the pilus, whereas the parental strain was associated with an 80% rate of pneumonia. Histopathological studies demonstrated that the fliC mutants caused very focal inflammation and that the organisms did not spread through the lungs as seen in infection due to either PAK or PAK/NP. Purified flagellin elicited an intense inflammatory response in the mouse lung. 125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay. However, flagellin-mediated binding to epithelial gangliosides was a relatively unusual event, as quantified by binding assays of wild-type or fliC mutant organisms to CHO Lec-2 cells with membrane-incorporated GM1. Fla+ organisms but not fliC mutants were efficiently taken up by murine macrophages. P. aeruginosa flagella are important in the establishment of respiratory tract infection and may act as a tether in initial interactions with epithelial membranes. This function is offset by the contribution of flagella to host clearance mechanisms facilitating phagocytic clearance and the role of flagellar genes in mucin binding and clearance.
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PMID:Role of flagella in pathogenesis of Pseudomonas aeruginosa pulmonary infection. 942 37

Pseudomyxoma peritonei (PMP) is an unusual form of intraabdominal neoplasm that produces a large amount of extracellular mucin. It is often associated with mucinous tumors of gastrointestinal tract or ovary. Herein, we report 3 patients with pseudomyxoma peritonei with high serum carbohydrate antigen 19-9 (CA19-9) levels. The first patient, who had a CA19-9 level of 1132 U/ml, had well-differentiated rectal cancer and died of chemotherapy complications, pneumonia and septic shock; one month after admission. The other 2 cases with CA19-9 levels of 2520 U/ml and 679 U/ml had tumors of unknown origins and had survived more than 1 year and 3 months after treatment, respectively. Usually, elevated serum CA19-9 levels are found in patients with pancreatic, biliary, colorectal, gastric or liver cancers. However, many studies have shown high serum CA19-9 levels are associated with mucinous carcinoma. Immunochemical studies also showed positive staining of CA19-9 in mucinous tumors. PMP is composed of large amounts of mucin, therefore, we suggest that serum and ascites CA19-9 levels should be routinely checked in patients with PMP.
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PMID:Pseudomyxoma peritonei with high serum CA19-9: report of three cases. 1041 16

To investigate pathophysiologies of Mycoplasma pneumoniae infection from an immunological point of view, we measured the levels of interleukin-18 (IL-18) (originally designated gamma interferon [IFN-gamma]-inducing factor) in 19 serum samples from 10 patients with pneumonia without pleural effusion (ages 1 to 16 years), 3 serum and 13 pleural fluid samples from 11 patients with pleural effusions (ages 11 months to 15 years), and 18 serum and 27 cerebrospinal fluid samples from 24 patients with central nervous system complications (ages 1 to 15 years). IL-18 was measured by a commercially available enzyme-linked immunosorbent assay kit (MBL, Nagoya, Japan). In addition, the levels of tumor necrosis factor alpha, IFN-gamma, IL-6, IL-12, and KL-6 (a mucin-like glycoprotein expressed on type 2 pneumocytes) were measured in selected samples. The results concerning pleural effusions showed that elevated levels of IL-18 in pleural fluid, but not in serum, were solely associated with a sustained fibrotic change of the lung on chest roentgenography which might represent a pathological feature of intraluminal organization. All the pleural fluid samples with elevated levels of IL-18 were positive by PCR for M. pneumoniae DNA. There was no association between IL-18 and IFN-gamma levels in serum or in the pleural fluid. On the other hand, elevated levels of IL-18 in serum, but not in cerebrospinal fluid samples, were observed in the cases complicated by central nervous system involvement, including profound brain dysfunction with seizures. Our study demonstrated that M. pneumoniae can induce IL-18 and that the enhanced local production of IL-18 in the lung is closely associated with pulmonary disease manifestation.
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PMID:Close association between pulmonary disease manifestation in Mycoplasma pneumoniae infection and enhanced local production of interleukin-18 in the lung, independent of gamma interferon. 1106 97

The antigen KL-6, a mucin-like high-molecular-weight glycoprotein, is expressed on type-2 pneumocytes and bronchiolar epithelial cells. Serum levels of KL-6 have been shown to correlate well with the activities of several different kinds of interstitial pneumonia. The purpose of this study was to assess the usefulness of monitoring serum KL-6 levels in patients who had received thoracic radiotherapy (TRT). In particular, the usefulness of such a protocol for the early diagnosis of severe radiation pneumonitis (RP) and the evaluation of its progress and severity was examined. Serum KL-6 levels were retrospectively monitored in 16 patients with lung cancer who had received TRT with or without chemotherapy. Eight of these patients had developed severe RP and eight had developed localized (within the irradiated field) RP. Serum KL-6 levels were measured using a modified sandwich-type enzyme-linked immunosorbent assay. In patients who developed severe RP, serum KL-6 levels showed a consistent tendency to increase after the clinical diagnosis of RP. In four patients, serum KL-6 levels even began to rise before a clinical diagnosis of severe RP had been made. In the patients with localized RP, on the other hand, the serum levels did not show any tendency to increase during or after TRT. Moreover, patients whose serum KL-6 levels rose more than 1.5 times higher than their pre-treatment serum KL-6 level, had a large chance of developing severe RP that was unresponsive to steroid hormones and resulted in death. Serum KL-6 levels, therefore, should be useful indicators for the early diagnosis of severe RP and for estimating its progress and severity in patients treated with TRT.
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PMID:Serum levels of KL-6 are useful biomarkers for severe radiation pneumonitis. 1155 24

The epidermal growth factor-seven transmembrane (EGF-TM7) family is a group of seven-span transmembrane receptors predominantly expressed by cells of the immune system. Family members CD97, EGF module-containing mucin-like receptor (EMR) 1, EMR2, EMR3, EMR4, and EGF-TM7-latrophilin-related protein are characterized by an extended extracellular region with a variable number of N-terminal EGF-like domains. EGF-TM7 receptors bind cellular ligands as demonstrated by the interaction of CD97 with decay accelerating factor (CD55) and dermatan sulfate. Investigating the effect of newly generated mAb on the migration of neutrophilic granulocytes, we here report for the first time in vivo data on the function of CD97. In dextran sulfate sodium-induced experimental colitis, we show that homing of adoptively transferred neutrophils to the colon was significantly delayed when cells were preincubated with CD97 mAb. The consequences of this defect in neutrophil migration for host defense are demonstrated in a murine model of Streptococcus pneumoniae-induced pneumonia. Mice treated with CD97 mAb to EGF domain 1 (1B2) and EGF domain 3 (1C5) displayed a reduced granulocytic inflammatory infiltrate at 20 h after inoculation. This was associated with a significantly enhanced outgrowth of bacteria in the lungs at 44 h and a strongly diminished survival. Together, these findings indicate an essential role for CD97 in the migration of neutrophils.
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PMID:The epidermal growth factor-seven transmembrane (EGF-TM7) receptor CD97 is required for neutrophil migration and host defense. 1470 87

A 74-year-old woman with chronic auricular fibrillation, arterial hypertension, hypercholesterolemia, ischemic cardiopathy, and peripheral arteriopathy presented with purpuric lesions on the lower limbs (Fig. 1) and, to a lesser extent, on the anterior area of the chest. The mucous membranes were not affected. In 1989, she was diagnosed with anemia that evolved until 1998, when a bone marrow biopsy revealed a myelodysplastic syndrome unclassified in French-American-British Group (FAB). The patient has required periodic transfusions since February 1999. A skin biopsy of the purpuric lesions revealed a leukocytoclastic vasculitis; the lesions cleared with topical corticosteroid treatment. In May 1999, the patient presented with inflammatory and painful lesions localized on the vulva (Fig. 2), which had evolved over several days, without fever. No lesions were observed in other locations. A cutaneous biopsy showed an intense dermal edema and a diffuse and polymorphous dermal infiltrate involving the follicular structures. Exocytosis, spongiosis, and mucin deposits, demonstrated by Alcian blue stain, were observed in the follicular epithelium. Mature neutrophils were predominant in the dermal infiltrate, but a small number of eosinophils and immature cells were also present (Fig. 3). The myelogenous origin of the immature lining cells was further confirmed by positive staining of intracytoplasmic granules with naphthol-ASD chloroacetate sterase (Leder's stain). Vasculitis was not observed. Routine laboratory tests revealed 3030 leukocytes/mm(3) (60% neutrophils), a hemoglobin level of 8.4 g/dL, and 92,000 platelets/mm(3). Treatment with 30 mg/day of prednisone was started, and the lesions cleared slowly within 4 weeks. A new bone marrow biopsy in September 1999 showed a similar appearance to that taken in 1998. The patient died in January 2000 as a result of pneumonia with cardiac and respiratory failure. A 66-year-old man presented with a febrile syndrome that had evolved over 5 days, and painful and pruritic cutaneous lesions on the face and posterior neck (Fig. 4). Three months before, the patient was diagnosed with chronic myelogenous leukemia in acceleration phase. Examination revealed an edematous and erythematous face with pustular lesions on the surface, also involving the neck and the upper part of the back. The histopathologic examination revealed an intense edema and abscesses in the dermis. The infiltrate of these lesions was composed of mature neutrophils with the presence of abundant immature cells with a myelogenous aspect (Fig. 5). Analytical studies revealed 26,130 leukocytes/mm(3) (42% blasts). No specific treatment for Sweet's syndrome was administered and the lesions showed an improvement within 5 days. Eight days after admission, the patient died as a result of acute hemorrhage, before treatment for leukemia was initiated.
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PMID:Concurrent Sweet's syndrome and leukemia cutis in patients with myeloid disorders. 1610 72

Mycoplasma hyopneumoniae is the causative agent of porcine enzootic pneumonia, a chronic and economically significant respiratory disease that affects swine production worldwide. M. hyopneumoniae adheres to and adversely affects the function of ciliated epithelial cells of the respiratory tract, and the cilium adhesin (Mhp183, P97) is intricately but not exclusively involved in this process. Although binding of pathogenic bacteria to glycosaminoglycans is a recognized step in pathogenesis, knowledge of glycosaminoglycan-binding proteins in M. hyopneumoniae is lacking. However, heparin and other sulfated polysaccharides are known to block the binding of M. hyopneumoniae to purified swine respiratory cilia. In this study, four regions within the cilium adhesin were examined for the ability to bind heparin. Cilium adhesin fragments comprising 653 amino acids of the N terminus and 301 amino acids of the C terminus (containing two repeat regions, R1 and R2) were cloned and expressed. These fragments bound heparin in a dose-dependent and saturable manner with physiologically significant binding affinities of 0.27 +/- 0.02 microM and 1.89 +/- 0.33 microM, respectively. Heparin binding of both fragments was strongly inhibited by the sulfated polysaccharides fucoidan and mucin but not by chondroitin sulfate B. When the C-terminal repeat regions R1 and R2 were cloned separately and expressed, heparin-binding activity was lost, suggesting that both regions are required for heparin binding. The ability of the cilium adhesin to bind heparin indicates that this molecule plays a multifunctional role in the adherence of M. hyopneumoniae to host respiratory surfaces and therefore has important implications with respect to the pathogenesis of this organism.
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PMID:Two domains within the Mycoplasma hyopneumoniae cilium adhesin bind heparin. 1636 4

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