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

An immunohistochemical analysis of Rhodococcus equi-induced pneumonia in 10 foals was performed by biotin-streptavidin system. The detection of R. equi was more sensitive in immuno-stain using anti-R. equi serum than in Gram's stain. This bacteria also reacted to anti-BCG serum. Lysozyme and alpha 1-antitrypsin were detectable in macrophages. A particularly intense staining was observed in association with intracellular bacteria. Though a degree of reaction for alpha 1-antichymotrypsin was very low in comparison with lysozyme and alpha 1-antitrypsin, it was also demonstrated in macrophages ingesting R. equi. These bacteria were almost intact under an electron microscope. Therefore, the surface components of R. equi may play important roles of protection from intracellular enzymes of macrophages. The cells containing intracytoplasmic IgM, IgG or IgA were a few in number and scattered predominantly around the pneumonic lesion. It is considered that the bactericidal activity by immunoglobulins may be weak in comparison with phagocytosis by macrophages.
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PMID:Immunohistochemical observations on pneumonic lesions caused by Rhodococcus equi in foals. 164 74

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41

Elevated levels of immunoreactive pancreatic secretory trypsin inhibitor (PSTI) were found in serum from patients with perforated duodenal ulcer, bacterial peritonitis, urosepticemia, pneumonia, acute renal failure, and also after different surgical procedures. The extent of the trauma seemed to determine the maximal level of PSTI. The increase found paralleled the changes seen in the acute-phase protein antichymotrypsin. There was, however, almost no increase in trypsinogen, thought to be produced together with PSTI in the acinar cells of the pancreas. In conclusion, there is evidence that PSTI is probably also produced somewhere outside the pancreas, in agreement with recent immunohistochemical data. This production may be part of a general acute-phase reaction. Thus, PSTI may have a more general inhibitory function against trypsin-like protease release in tissue injury, instead of being a purely local trypsin inhibitor in the pancreatic gland.
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PMID:Elevated pancreatic secretory trypsin inhibitor levels during severe inflammatory disease, renal insufficiency, and after various surgical procedures. 381 2