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)

Vascular cell adhesion molecule-1 (VCAM-1) is expressed by endothelial cells in a variety of inflammatory conditions in experimental animals and humans. It is increased in rabbit endothelium after the intravenous administration of endotoxin, after cholesterol feeding, in regeneration after injury, and in alloxan-induced diabetes mellitus. The effect of a respiratory tract infection with Pasteurella multocida, a common laboratory pathogen in rabbits, on VCAM-1 expression by aortic endothelial cells and on the endothelial ultrastructure was examined in specific-pathogen-free (SPF) New Zealand White rabbits infected by the instillation of a suspension of live organisms into the nose and in conventionally raised rabbits with naturally acquired P. multocida infection. Age-matched SPF rabbits maintained in a disease-free environment were controls. Rabbits were euthanized 50 days after infection, the aorta was excised, and the endothelial cells expressing VCAM-1 were identified by immunohistochemistry. Perfusion-fixed aortas from infected and SPF rabbits were prepared for examination by electron microscopy. All infected animals had pneumonitis and leukocytosis. In SPF rabbits the total leukocyte count was highest at postinfection day 25. There was a significant (P < 0.05) increase in the number of VCAM-1-positive aortic endothelial cells in infected SPF rabbits (34 +/- 4/10(4) endothelial cells; n = 5) and rabbits with naturally acquired infection (57 +/- 14/10(4) endothelial cells; n = 5) compared with control animals (12 +/- 3 per 10(4) endothelial cells; n = 4). The endothelium of infected rabbits had morphologic alterations consistent with injury. Thus infection at remote sites can activate arterial endothelium and induce the expression of VCAM-1.
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PMID:Increased expression of vascular cell adhesion molecule-1 by the aortic endothelium of rabbits with Pasteurella multocida pneumonia. 905 44

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

This study tested the hypothesis that very late antigen (VLA)-4 mediates CD18-independent neutrophil emigration into the airspaces induced by either Streptococcus pneumoniae, a stimulus that induces primarily CD18-independent neutrophil emigration, or Escherichia coli, toward which only 20-30% of the total number of neutrophils emigrate through CD18-independent pathways. In wild-type (WT) mice, VLA-4 expression was less on neutrophils that emigrated into the airspaces than on circulating neutrophils. Vascular cell adhesion molecule-1 (VCAM-1) mRNA, the major endothelial cell ligand for VLA-4, increased more in E. coli than in S. pneumoniae pneumonia. VCAM-1 protein expression was not detected in capillaries, the major site of neutrophil emigration. Neutrophil emigration during E. coli or S. pneumoniae pneumonia was similar in mice given antibodies against both CD18 and VLA-4 compared with mice given the anti-CD18 antibody and a control antibody. However, in hematopoietically reconstituted mice with both WT and CD18-deficient neutrophils in their blood, the migration of CD18-deficient neutrophils in response to S. pneumoniae was slightly but significantly less in animals pretreated with the anti-VLA-4 antibody than in those receiving a control antibody. These data suggest that VLA-4 plays a small role in CD18-independent neutrophil emigration, but the majority of CD18-independent neutrophil emigration induced by bacteria in the lungs occurs through VLA-4-independent mechanisms.
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PMID:Very late antigen-4 in CD18-independent neutrophil emigration during acute bacterial pneumonia in mice. 1209 Nov 71

Recruitment of neutrophils into the alveoli plays a major role in the pathogenesis of acid-induced pneumonitis. Preliminary data suggest that alteration in the expression of cellular adhesion molecules on the airway epithelial cells may play an important role in the recruitment of neutrophils following acid-induced lung injury. The aim of this study was to evaluate the change in the surface expression of intercellular adhesion molecule-1 (ICAM-1), E-cadherin, and vascular cell adhesion molecule -1 (VCAM-1) on acid-exposed A549 alveolar lining epithelial cells by flow cytometry and confocal laser microscopy. Acid exposure changed cell morphology, increased cell adhesion after trypsin-EDTA treatment, and up-regulated the expression of ICAM-1 and E-cadherin but not of VCAM-1. The up-regulation of ICAM-1 expression will induce the dysfunction of epithelial cells with or without accumulation of neutrophils in air spaces. Because the distribution of E-cadherin in acid-exposed A549 cells was at the sites where the cells attached to culture dish but not at the intercellular junctions between adjoining cells, up-regulated expression of E-cadherin will rather result in alterations of epithelial morphology and function of epithelial barrier. In addition, pentoxifylline suppressed the up-regulation of ICAM-1 and E-cadherin expression and may therefore attenuated the airway inflammation in acid-induced pneumonitis.
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PMID:Acid exposure potentiates intercellular adhesion molecule-1 and e-cadherin expression on A549 alveolar lining epithelial cells. 1288 51

Asthma is a disease characterized by chronic airway inflammation, and Th2 cells play a critical role in initiating and sustaining asthmatic inflammation. It has been shown that CD44 expressed on CD4(+) T cells plays a critical role in the accumulation of antigen-specific Th2 cells in the development of airway hyperresponsiveness induced by antigen challenge in the airways. The aim of this study was to determine whether there are specific CD44 variant isoforms (CD44v) expressed on lymphocytes from asthmatic patients. We collected whole blood samples from 103 normal subjects, 165 subjects with asthma and 104 with pneumonia. Peripheral blood lymphocyte isolation was performed, and total RNA was extracted from the isolated lymphocytes, using nested PCR for specific CD44v amplification on lymphocytes. Demographic variables were analyzed using linear regression in order to determine whether the expression of CD44v was correlated with these demographic features. The nested PCR results revealed that CD44v5 was expressed by 55.2% of asthma patients, which was significantly higher than levels of expression in the other groups. Lower percentages of individuals in the normal subject group exhibited expression of CD44v5 and CD44v6. The data demonstrated that the percentage of individuals in the pneumonia group expressing CD44v5 was 29.0%, but a higher percentage of these patients expressed CD44v6. CD44v5 expression was positively correlated with IgE levels (p=0.032) in the asthmatic patient group, and CD44v6 was significantly positively correlated with the neutrophil count (p<0.05). CD44v5 was expressed by a higher proportion of asthmatic patients than other subjects and thus may play an important role in the pathogenesis of asthma. These findings may offer a new target for the diagnosis and treatment of asthma and may also provide insights into the mechanisms of asthma development.
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PMID:CD44 variant isoforms are specifically expressed on peripheral blood lymphocytes from asthmatic patients. 2306 Sep 26

Luteolin, an anti-inflammatory ingredient found in the Chinese herb Folium perillae, can inhibit not only the cyclic adenosine monophosphate (cAMP)-phosphodiesterases (PDEs) activity of neutrophils, but also the expression of lymphocyte function-associated antigen-1 in neutrophils, both of which result in a decrease in the adhesion between neutrophils and microvascular endothelial cells. However, the effect of luteolin on the cAMP-PDEs activity and expression of adhesion molecules in endothelial cells are not clear. In the present study, primary rat pulmonary microvascular endothelial cells and a lipopolysaccharide-induced rat acute pneumonia model were used to explore the role of luteolin on cAMP-PDEs activity, expression of adhesion molecules, and leukocyte infiltration. We demonstrate that rat pulmonary microvascular endothelial cells expressed high levels of cAMP-PDEs, specifically PDE4, and further luteolin exhibited dose-dependent inhibition on the activity of cAMP-PDEs or PDE4 in endothelial cells. Luteolin also had a significant inhibitory effect on the expression of vascular cell adhesion molecule (VCAM)-1, but not intracellular cell adhesion molecule (ICAM)-1 in microvascular endothelial cells. Further, we show that luteolin decreased the levels of soluble ICAM-1 (sICAM-1), but not soluble E-selectin in the serum of rats subjected to acute pneumonia. We also show that luteolin treatment decreased the wet/dry weight ratio of lung tissue and reduced the total number of serum leukocytes in a dose-dependent manner in a rat acute pneumonia model. In conclusion, these results demonstrate that luteolin suppresses inflammation, at least in part, through inhibiting both cAMP-PDEs or PDE4 activity and the expression of VCAM-1 (in vitro) and sICAM-1 (in vivo) in endothelial cells.
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PMID:Luteolin suppresses inflammation through inhibiting cAMP-phosphodiesterases activity and expression of adhesion molecules in microvascular endothelial cells. 3027 58