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)

An imbalance of proteolytic enzymes and protease inhibitors may contribute to the development of bronchopulmonary dysplasia. We studied secretory leukocyte protease inhibitor (not previously addressed), and alpha 1-antitrypsin, alpha 1-antichymotrypsin, alpha 2-macroglobulin and elastase. Albumin was used as an internal reference. Infants with pneumonia had higher concentrations of secretory leukocyte protease inhibitor (p = 0.02) and elastase (p = 0.04) in bronchoalveolar lavage fluid than those with respiratory distress syndrome; those who also developed bronchopulmonary dysplasia had intermediate values. A decreased concentration of alpha 1-antitrypsin was found in the second and third postnatal weeks (p = 0.002). Further detailed studies of the balance between proteases and protease inhibitors and of the importance of pulmonary infections in the pathogenesis of bronchopulmonary dysplasia are suggested. Secretory leukocyte protease inhibitor is important both as an elastase inhibitor of bronchial mucus and as a marker of infection in the bronchi.
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PMID:Protease inhibitors in bronchoalveolar lavage fluid from neonates with special reference to secretory leukocyte protease inhibitor. 138 26

Alpha 2-beta 1-glycoprotein may be found free in horse serum or complexed with alpha-1-proteinase inhibitor to form pre-alpha 2-elastase inhibitor. There has been little information published concerning alpha 2-beta 1-glycoprotein and its possible tissue sources in horses. A peroxidase-antiperoxidase technique was used to identify alpha 2-beta 1-glycoprotein in buffy coat and bone marrow neutrophils of healthy horses. Macrophages and neutrophils in bronchoalveolar lavage samples from clinically normal horses and from horses with chronic pulmonary disease also were positive for alpha 2-beta 1-glycoprotein. Alpha 2-beta 1-glycoprotein was identified in some instances in normal equine hepatocytes of formalin-fixed liver sections. In formalin-fixed lung sections from horses with chronic, small-airway disease and chronic bronchointerstitial pneumonia, alpha 2-beta 1-glycoprotein was observed in some airway secretions and in macrophages.
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PMID:Immunohistochemical localization of alpha 2-beta 1-glycoprotein in horses. 208 28

We report a rare case of acute respiratory distress syndrome (ARDS) induced by Influenza A (H3 N2) without secondary microbiological infection. A 69-year-old woman was admitted to our hospital because of cough and severe dyspnea. We diagnosed ARDS, because of the severe respiratory failure resistant to high-dose oxygen, the diffuse bilateral infiltrates without cardiomegaly on chest radiography, and the normal pulmonary artery wedge pressure. This patient was treated with high doses of methylprednisolone, antibiotics, globulins, urinastatin, neutrophilic elastase inhibitor, nitric oxide inhalation, and extracorporeal membrane oxygenation, but died on the thirteenth hospital day. Our final diagnosis was ARDS induced by fulminant influenza (A/Hong Kong/68 (H3 N2)) virus pneumonia, because the antibody titers of H3 N2 influenza of paired sera showed a 128-fold increase.
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PMID:[A case of acute respiratory distress syndrome induced by fulminant influenza A (H3 N2) pneumonia]. 1118 25

The control of lung inflammation is of paramount importance in a variety of acute pathologies, such as pneumonia, the acute respiratory distress syndrome, and sepsis. It is becoming increasingly apparent that local innate immune responses in the lung are negatively influenced by systemic inflammation. This is thought to be due to a local deficit in cytokine responses by alveolar macrophages and neutrophils following systemic bacterial infection and the development of a septic response. Recently, using an adenovirus-based strategy which overexpresses the human elastase inhibitor elafin locally in the lung, we showed that elafin is able to prime lung innate immune responses. In this study, we generated a novel transgenic mouse strain expressing human elafin and studied its response to bacterial lipopolysaccharide (LPS) when the LPS was administered locally in the lungs and systemically. When LPS was delivered to the lungs, we found that mice expressing elafin had lower serum-to-bronchoalveolar lavage ratios of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), macrophage inflammatory protein 2, and monocyte chemoattractant protein 1, than wild-type mice. There was a concomitant increase in inflammatory cell influx, showing that there was potential priming of innate responses in the lungs. When LPS was given systemically, the mice expressing elafin had reduced levels of serum TNF-alpha compared to the levels in wild-type mice. These results indicate that elafin may have a dual function, promoting up-regulation of local lung innate immunity while simultaneously down-regulating potentially unwanted systemic inflammatory responses in the circulation.
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PMID:Regulation of pulmonary and systemic bacterial lipopolysaccharide responses in transgenic mice expressing human elafin. 1281 58