Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Few molecules are active against respiratory viruses. In upper respiratory tract infections, which are frequent and fortunately not severe, their deficiency is not a problem. However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor: anti-receptor antibodies, soluble ICAM-1, capsid-binding agents. The lower respiratory tract infections (bronchiolitis, pneumonia...), mainly due to respiratory syncytial virus and influenza viruses are potentially more severe, and 2 groups of compounds are or have been used in these infections: amantadine and ribavirin. Ribavirin is effective in respiratory infections due to respiratory syncytial, influenza and parainfluenza viruses, and on many other viruses. Its toxicity needs to administrate it as an aerosol, and in France, ribavirin is used as compassional treatment in severe forms of bronchiolitis or pneumonia due to respiratory syncytial virus, and in high-risk children. Anti-parkinsonian drugs, related to amantadine (Mantadix, Roflual) are no longer on sale. Therefore there is no active molecule yet available against these viruses.
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PMID:[Drugs active against respiratory viruses]. 918 39

Inflammatory cell infiltration of the lung is a predominant histopathological change that occurs during radiation pneumonitis. Emigration of inflammatory cells from the circulation requires the interaction between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. We studied the immunohistochemical pattern of expression of cell adhesion molecules in lungs from mice treated with thoracic irradiation. After X-irradiation, the endothelial leukocyte adhesion molecule 1 (ELAM-1; E-selectin) was primarily expressed in the pulmonary endothelium of larger vessels and minimally in the microvascular endothelium. Conversely, the intercellular adhesion molecule 1 (ICAM-1; CD54) was expressed in the pulmonary capillary endothelium and minimally in the endothelium of larger vessels. Radiation-mediated E-selectin expression was first observed at 6 h, whereas ICAM-1 expression initially increased at 24 h after irradiation. ICAM-1 and E-selectin expression persisted for several days. P-selectin is constitutively expressed in Weibel-Palade bodies in the endothelium, which moved to the vascular lumen within 30 min after irradiation. P-selectin was not detected in the pulmonary endothelium at 6 h after irradiation. The radiation dose required for increased cell adhesion molecule expression within the pulmonary vascular endothelium was 2 Gy, and expression increased in a dose-dependent manner. These data demonstrate that ICAM-1 and E-selectin expression is increased in the pulmonary endothelium following thoracic irradiation. The pattern of expression of E-selectin, P-selectin, and ICAM-1 is distinct from one another.
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PMID:Ionizing radiation mediates expression of cell adhesion molecules in distinct histological patterns within the lung. 918 1

In an asymptomatic 4 yr old child with radiographic evidence of parenchymal lung disease, bronchoalveolar lavage (BAL) yielded the diagnosis of chronic lipid pneumonia caused by chronic aspiration of mineral oil given as a laxative. BAL analysis showed a marked reduction in the total number of alveolar macrophages; almost 70% of these cells contained intracytoplasmic lipid vacuoles. It also disclosed lymphocytic (cytotoxic/suppressor) alveolitis. A high percentage of lymphocytes expressed antigen markers of activation (human leucocyte antigen (HLA)-DR), CD54 and CD25). BAL analysis 18 months after mineral oil intake revealed that lymphocytes bearing antigen markers of activation had markedly decreased whereas alveolar macrophages (normal and lipid-laden) had increased. A subsequent whole lung BAL was considered unnecessarily invasive in this otherwise healthy child.
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PMID:Bronchoalveolar lavage cell analysis in a child with chronic lipid pneumonia. 954 99

Elevated levels of air pollution particulates < or = 10 microm in diameter (PM10) have been associated with an increase in mortality and morbidity due to pulmonary complications, including pneumonia. Impairment of inflammatory and host defense functions of the alveolar macrophage (AM) may be a precipitating factor. The present study was undertaken to determine whether human AM and blood derived monocytes (MO) modulate the expression of receptors important for phagocytosis of opsonized microbes (CD11b, CD11c), gram-negative bacteria (CD14), extracellular matrix interaction (CD29), and immune responses (CD11a, CD54, HLA-DR) when exposed to particulates obtained from urban air (UAP). Furthermore, phagocytosis of and oxidant generation by opsonized yeast were investigated in particle-exposed cells. AM and MO exposed to UAP for 18 h expressed significantly lower levels of CD11b and CD29. CD14 expression was markedly decreased in MO but not in AM, and CD11c was reduced in AM but not in MO. CD11a, CD54, and HLA-DR were unaltered in both phagocyte populations. Decreased receptor expression was not dependent on particle load in the cells. Phagocytosis of Saccharomyces cerevisiae and the chemiluminescence response were also significantly inhibited by UAP. Time-course studies revealed that decreased oxidant generation was evident already at 3 h postexposure, while significant effects on phagocytosis and CD11b expression were found at 18 h. These data indicate that exposure to particulate pollution is likely to impair host defense functions of AM and MO, which are important in elimination of a variety of pathogens in the lung.
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PMID:Decreased CD11b expression, phagocytosis, and oxidative burst in urban particulate pollution-exposed human monocytes and alveolar macrophages. 986 Mar 21

It was hypothesized that there would be an upregulation of systemic neutrophil CD11b expression in pneumonia. Expression of CD11b and concentrations of soluble intercellular adhesion molecule (ICAM)-1 and E-selectin were evaluated as potential surrogate markers of the severity of pneumonia. Possible age-related immunosenescence in relation to neutrophil CD11b expression in elderly patients with pneumonia was examined for. In patients with community-acquired pneumonia (n = 36) neutrophil CD11b expression was measured by flow cytometry and soluble ICAM-1 and E-selectin concentrations by enzyme-linked immunosorbent assay. An upregulation of neutrophil CD11b expression and increased soluble adhesion molecule concentrations on admission were confirmed, but the concentrations did not correlate with patient Acute Physiology and Chronic Health Evaluation II scores. Neutrophil CD11b expression was similar between elderly (age range 70-100 yrs) and younger (age range 18-70 yrs) patients with pneumonia. In conclusion, there is evidence of neutrophil and endothelial cell activation in pneumonia as indicated by upregulation of CD11b and increased soluble intercellular adhesion molecule and E-selectin, however, they do not appear to be good surrogate markers of severity of infection. Advanced age does not influence adhesion molecule expression in pneumonia.
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PMID:Neutrophil CD11b and soluble ICAM-1 and E-selectin in community acquired pneumonia. 1044 15

Tumour necrosis factor-alpha (TNF) plays a central role in the recruitment and activation of mononuclear cells in mycobacterial infection. In the absence of type 1 TNF receptor, Mycobacterium bovis Bacillus Calmette-Guerin (BCG) infection of mice is not contained, leading to fatal disease. Because type 1 TNF receptor binds both TNF and lymphotoxin-a, we used TNF-deficient mice to determine the specific role of TNF in the host resistance to BCG infection. The bacterial burden of the lungs of TNF-deficient mice was substantially increased and the mice succumbed to pneumonia between 8 and 12 weeks with a defective granuloma response. Atypical granulomas developed by 4 weeks expressing low levels of MHC class II, intracellular adhesion molecule (ICAM-1), CD11b and CD11c. Macrophages showed little signs of activation and had low levels of acid phosphatase activity and inducible nitric oxide synthase (INOS) expression. Despite the defective cellular recruitment, the chemokines, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1alpha), were increased in broncho-alveolar lavage fluid of TNF-deficient mice. The defective host response was corrected by the transplantation of normal bone marrow cells into irradiated TNF-deficient mice. These results demonstrate that TNF derived from hemopoietic cells rather than from mesenchymal origin are essential for a normal host response to BCG infection. Furthermore, TNF dependent expression of adhesion molecules may be essential for the recruitment of mononuclear cells for the formation of bactericidal BCG granulomas.
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PMID:Correction of defective host response to Mycobacterium bovis BCG infection in TNF-deficient mice by bone marrow transplantation. 1087 41

We report here a case of interstitional pneumonia (IP) associated with amyopathic dermatomyositis (DM). In August, 1998, a 53-year-old Japanese man was admitted to our hospital because of fever, polyarthritis and erythematous heliotrope eruption and Gottron's sign without any symptom of myositis. Serum CK level and EMG were normal. Jo-1 antibody was negative. Chest computed tomography (CT) revealed IP at both lung base areas. The patient was diagnosed as amyopathic DM with IP. When IP rapidly progressed, methylprednisolone pulse therapy and oral high dose prednisolone were not effective. High-dose intravenous cyclophosphamide seemed to be transiently effective, but oral cyclosporine A was not effective. The patient was died of respiratory failure in October 1998. During the course, we measured serum levels of LDH, sIL-2 R, s-ICAM-1 and KL-6, KL-6 could be a sensitive parameter of IP activity.
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PMID:[A case of amyopathic dermatomyositis with rapidly progressive interstitial pneumonia]. 1102 Nov 75

Following allogeneic bone marrow transplantation (alloBMT), idiopathic pneumonia syndrome (IPS) and graft-versus-host disease (GVHD) caused by donor cell alloreactivity remain major obstacles to a successful outcome. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that is involved in regulating lymphohematopoietic cell migration and facilitating T-cell responses. To determine whether ICAM-1 expression in the host would affect IPS or GVHD tissue injury responses, ICAM-1(-/-) mice were compared with ICAM-1(+/+) controls. ICAM-1(-/-) recipients did not exhibit the manifestations of IPS injury such as an increase in lung weights nor decreased lung function. The influx of T cells, macrophages, and neutrophils was dramatically dampened as was the production of the inflammatory cytokines interferon-gamma and tumor necrosis factor alpha and the chemokines monocyte chemotactic protein 1, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and lymphotactin, normally upregulated in the lung during IPS. In contrast, systemic levels of these mediators were unaffected and GVHD-induced lesions in the liver and colon did not differ in severity regardless of ICAM-1 expression. GVHD-mediated mortality was accelerated in ICAM-1(-/-) recipients at doses of allogeneic spleen cells that are otherwise not uniformally lethal. These data implicate ICAM-1 as playing a critical role in the generation of IPS; therefore, ICAM-1 may be a discerning element, segregating IPS from GVHD injury post-alloBMT.
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PMID:Intercellular adhesion molecule-I (ICAM-I, CD54) deficiency segregates the unique pathophysiological requirements for generating idiopathic pneumonia syndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation. 1152 86

We compared six inflammatory mediators (C-reactive protein (CRP), interleukin-6 (IL-6), soluble tumour necrosis factor receptors (p55 and p75) and soluble adhesion molecules (ICAM-1, E-selectin)) as early diagnostic tests for neonatal sepsis, and studied the possible benefit of combining parameters. Blood samples were obtained from 166 consecutively admitted neonates, who were suspected to suffer from infection within the first week of life. Neonates were retrospectively classified as infected (sepsis, clinical sepsis or pneumonia), possibly infected, or non-infected. Twenty-four infected neonates had higher serum levels of all six mediators (all P < 0.05), and 18 possibly infected neonates had higher levels of CRP, IL-6, ICAM-1 and E-selectin (all P < 0.05), than neonates without infection (n = 124). Receiver operator characteristic plots showed that CRP was the single best diagnostic test. Multiple logistic regression modelling, including various combinations of two to six mediators, consistently showed that IL-6, in addition to CRP, predicted sepsis. With infected and possibly infected neonates as the reference standard, a combined test of CRP > or = 10 mg/l and/or IL-6 > or = 20 pg/ml had a sensitivity of 85%, specificity of 62%, and negative likelihood ratio of 0.24. Using infected neonates as reference standard alone, and including possibly infected as controls, sensitivity increased to 96%, whereas specificity decreased to 58%; a negative test result (CRP < 10 mg/l and IL-6 < 20 pg/ml) ruled out sepsis with high certainty (likelihood ratio = 0.07). CRP performed best as a diagnostic test for neonatal sepsis. Diagnostic accuracy was further improved by combining CRP and IL-6, whereas the other parameters (p55, p75, ICAM-1 and E-selectin) added no further diagnostic information.
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PMID:Early diagnostic markers for neonatal sepsis: comparing C-reactive protein, interleukin-6, soluble tumour necrosis factor receptors and soluble adhesion molecules. 1175 Jan 94

Recruitment of neutrophils into alveolar air spaces is an early event in the pathogenesis of pneumonia due to Streptococcus pneumoniae. This results from chemokines released by activated endothelial and epithelial cells and alveolar macrophages. Culture supernatants of 6 wild-type strains of S. pneumoniae, shown to contain choline-binding protein A (CbpA; clades A and B), induced release of chemokine CXCL8 from the human alveolar epithelial cell line A549, whereas a CbpA deletion mutant elicited significantly reduced CXCL8 release, compared with that of its isogenic parent (P<.01). Recombinant CbpA up-regulated expression of messenger RNA of CXCL8 and CCL2 but not of XCL1, CXCL10, CCL1, CCL3, CCL4, or CCL5 in A549 cells and induced increased secretion of CXCL8, CCL2, CXCL1, and CXCL5 in a dose- and time-dependent manner. CbpA also increased the expression of intercellular adhesion molecule 1 (CD54) by A549 cells. Thus, CbpA of S. pneumoniae induces the transcription and release of proinflammatory molecules by human alveolar epithelial cells.
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PMID:Choline-binding protein A of Streptococcus pneumoniae elicits chemokine production and expression of intercellular adhesion molecule 1 (CD54) by human alveolar epithelial cells. 1240 94


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