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)

Using a peroxidase anti-peroxidase technique alpha-1-protease inhibitor (alpha-1-PI) was identified in normal equine hepatocytes in formalin-fixed liver sections, and in airway secretions and macrophages in formalin-fixed lung sections of horses with chronic small airway disease and chronic bronchointerstitial pneumonia. In addition, it was identified occasionally in macrophages in bronchoalveolar lavage samples from clinically healthy horses and from horses with chronic small airway disease. Equine peripheral blood leucocytes and formalin-fixed lung sections with normal histology were negative for alpha-1-PI.
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PMID:Immunohistochemical localisation of alpha-1-protease inhibitor in the horse. 247 58

Impaired fibrinolysis may contribute to development of adult respiratory distress syndrome (ARDS). Pathologic increases in endogenous plasminogen activator inhibitor (PAI-1) may blunt normal fibrinolysis and unmask alternate fibrinolytic mechanisms, such as elastase-induced fibrin degradation. We measured PAI-1 and elastase-induced fibrin(ogen) degradation products in 69 critically ill patients in our medical intensive care unit (MICU) and in nine healthy volunteers. Factor VIII-related antigen protein (VIII:Ag), a reported marker of acute lung injury, and alpha-1-protease inhibitor (alpha-1-PI), an acute phase reactant, were also measured. MICU patients included 24 control patients with no known risk of ARDS, 35 patients with risk factors for ARDS including sepsis, pneumonia, aspiration, and shock, and 12 patients with ARDS including two patients from at-risk groups who developed ARDS. Plasma PAI-1 was determined by chromogenic assay, elastase-induced peptides by a new radioimmunoassay, VIII:Ag by immunoelectrophoresis, and alpha-1-PI by immunodiffusion. When compared to normal volunteers, MICU control patients had elevated PAI-1, VIII:Ag, elastase-induced peptides, and alpha-1-PI. Patients with ARDS had significantly higher PAI-1 and VIII:Ag than did MICU control patients; elastase-induced peptides and alpha-1-PI were not higher. However, at-risk patients who did not develop ARDS also had high PAI-1 or VIII:Ag. Although these data cannot refute the possible role of these compounds in the pathogenesis of ARDS, they demonstrate that PAI-1 and VIII:Ag may be elevated in many critically ill patients but may not be useful markers for the subsequent development of ARDS.
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PMID:Fibrinolysis in critically ill patients. 250 87

Eglin C is an inhibitor of polymorphonuclear leukocyte elastase and cathepsin G. Recently, it was suggested that Eglin C may inhibit bacterial clearance in an experimental animal model of pneumonia. Since the phagocytic-bactericidal activity of polymorphonuclear leukocytes is most important in the promotion of bacterial clearance, we determined the effect of Eglin C on a variety of functions of isolated human polymorphonuclear leukocytes such as phagocytic-bactericidal activity, superoxide production, degranulation and chemotaxis. Apart from a partial inhibition of superoxide production, which was shown to be due to a superoxide dismutase-like effect of Eglin C, there was no inhibition of polymorphonuclear leukocyte functions measured. Eglin C can therefore be considered as a protease inhibitor, which does not interfere with the phagocytic-bactericidal activity of human polymorphonuclear leukocytes.
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PMID:The effect of Eglin C on the function of human neutrophils in vitro. 285 14

The protease inhibitor leupeptin prevented multiple step replication of an influenza virus (A/swine/1976/31, H1N1) mediated by staphylococcal proteases. It also suppressed virus replication and development of fatal pneumonia in mice co-infected with the virus and Staphylococcus aureus.
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PMID:Inhibitory effect of a protease inhibitor, leupeptin, on the development of influenza pneumonia, mediated by concomitant bacteria. 329 42

Less than half of the paediatric HIV infections recorded in Australia have resulted from perinatal transmission, but in recent years this has been the predominant mode of infection. There are 136 infants who are known to have been exposed perinatally to HIV in Australia: 49 of these are infected. Caesarean section is thought now not to reduce the risk of perinatal transmission (PNT); rather, the risk increases with duration of membrane rupture and rises rapidly after 4 h of membrane rupture. However, no data exist to show that interventions to expediate delivery after membrane rupture reduce the risk of PNT. Data such as these suggest that the majority of perinatal infections (probably about 60%) occur close to the time of delivery. While the overall risk of PNT for non-breast fed infants is approximately 20-25%, the risk of infection for the infant is considerably increased when there is evidence of increased maternal viral burden. Advanced maternal disease predicts that if the infant is infected there is more likely to be early progression of HIV than is the case for the less frequently infected infants of mothers who are asymptomatic. Bottle feeding may prevent infection of 10% of children exposed perinatally. Use of zidovudine by the mother in the third trimester and i.v. zidovudine during labour, followed by oral zidovudine for the infant for 6 weeks can reduce the PNT rate by two thirds, to about 8%. Approximately 3% of uninfected infants with perinatal HIV exposure may be found to be transiently virus positive but eventually become antibody negative and thus appear to have eliminated the virus. The risk of Pneumocystis carinii pneumonitis (PCP) cannot be predicted on the basis of CD4 count and it is recommended that all children of infected mothers commence PCP prophylaxis around the age of 6 weeks-2 months and continue that therapy until the age of 12 months or until it becomes clear that the infant is uninfected. The cumulative risk of AIDS increases rapidly during the first year of life to about 20%, then more slowly at a rate of about 2 or 3% a year. The shape of this curve reveals the bimodal progression of HIV disease in children. About 15-20% of children rapidly develop a severe immune deficiency, opportunistic infections and, in most cases, encephalopathy. There is a very high morbidity rate in this group of children, most of whom die before the age of 3 or 4 years. In contrast, 80-85% of children only become immunodeficient after a relatively long period, which is similar to or perhaps even longer than that in adults. Recent studies indicate that zidovudine antiviral monotherapy is no longer appropriate. While no clear alternative to monotherapy has emerged most would, wherever possible, commence antiretroviral therapy with a combination of two or three drugs including zidovudine plus didanosine or lamivudine. If a third drug is used it would probably be a protease inhibitor.
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PMID:Paediatric HIV update. 940 77

Recent advances in the chemotherapeutic agents against HIV enabled us to conduct combination therapies using two nucleoside reverse transcriptase inhibitors and a protease inhibitor. The three-drug combination chemotherapies have been shown to be very potent in inhibiting HIV replication; they markedly suppress plasma HIV-RNA levels, elevate CD4 counts, reduce opportunistic infections and prolong survival of the patients. Early and hard treatment is now recommended. Among opportunistic infections in patients with HIV infection/AIDS, most frequent are respiratory tract infections including Pneumocystis carinii pneumonia, bacterial pneumonia, pulmonary tuberculosis, CMV pneumonia and fungus infections. Sensitivity and specificity of PCR method to detect Pneumocystis carinii are much better than the conventional Grocott stain of sputa. Early diagnosis of tuberculosis and atypical mycobacteriosis became possible using PCR and other molecular technology. Multi-drug resistant tuberculosis is fortunately rare among Japanese HIV-positive patients. Early and correct diagnosis of opportunistic infections markedly improves the prognosis of the patients.
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PMID:[HIV Infection/AIDS and respiratory tract infections in Japan]. 979 9

The introduction of protease inhibitors (PIs) gave a dramatic drop in AIDS-related opportunistic events, mainly due to induced immune reconstitution. Discontinuation of prophylaxis against Pneumocystis carinii is considered safe when CD4 > 200 cells/mm(3). Ideally, we should have specific functional tests for HIV-1-related decisions. We examined viro-immunological profiles, clinical outcome and lymphocyte proliferation (LP) to P. carinii and other antigens in 108 subjects: 28 AIDS presenters with P. carinii pneumonia (PCP) (CD4 < 200 cells/mm(3)), 22 untreated asymptomatic HIV-1-infected patients (CD4 > 200 cells/mm(3)), 44 HIV-1-infected patients immune-reconstituted on antiretroviral regimens and 14 HIV-1-uninfected healthy controls. As regards viral load, there was no significant difference in therapy duration, nadir, or actual CD4, CD8, natural killer or B cell counts in immune-reconstituted patients receiving protease inhibitor (PI)-based versus those receiving PI-sparing antiretroviral regimens. Among subjects showing abnormally low P. carinii-specific LP, three patients receiving a non-nucleoside reverse transcriptase inhibitor (nNRTI) developed PCP despite having CD4 > 250 cells/mm(3). P. carinii-specific LP could be considered for doubtful situations, i.e. for a safer clinical decision of discontinuing or restarting prophylaxis in patients with a low CD4 nadir or experiencing a sudden CD4 decrease under highly active antiretroviral therapy (HAART). HIV-1 PIs, having in vitro aspecific effects against Pneumocystis, could play a clinically significant anti-opportunistic role, thus offering a further benefit in heavily immunosuppressed patients during early stages of antiretroviral therapy.
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PMID:Assessment of immune reconstitution to Pneumocystis carinii in HIV-1 patients under different highly active antiretroviral therapy regimens. 1283 36

Gabexate mesilate is a synthetic protease inhibitor that is effective for acute pancreatitis. The effect of gabexate mesilate in influenza pneumonia in mice was investigated by examining the changes in pulmonary inflammatory cytokines and chemokines. Pathological changes in the lungs of treated mice were extremely mild, compared with changes in infected, untreated mice. Intrapulmonary levels of interleukin-6 and macrophage inflammatory protein-2 decreased in treated mice compared with untreated mice, despite similar viral titres in the lungs. Survival terms for treated and untreated groups were similar. These data indicate that gabexate mesilate has beneficial effects on influenza pneumonia, which may be due to the modulation of inflammatory cytokine/chemokine responses.
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PMID:Gabexate mesilate suppresses influenza pneumonia in mice through inhibition of cytokines. 1838 Sep 43

We studied the influence of a way of introduction proteinase inhibitors on efficiency of suppression of proteolysis activation during pneumonia. Comparative study of efficiency of proteases inhibition in experimental pneumonia has shown higher efficacy of local introduction of drugs. Intravenous and intraperitoneal introduction of proteinase inhibitors exhibited inhibitory effect of a smaller degree on local and systemic proteases activation, did not decrease an acute phase of response of alpha-1-protease inhibitor in comparison with endotracheal instillation of Contrycal and Ingiprol. The study has established that endotracheal introduction of proteinase inhibitors is the most effective for correction of the proteinase-inhibitor balance. It also helps to promote the activity proteinase-inhibitor, suppresses elastolytic activity, decreases cellular infiltration, reduces the concentration of proteins in bronco-alveolar lavage fluid that is connected with address delivery of drugs to the target organ creating a maximal concentration of drugs in affected area.
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PMID:[Effect of proteinase inhibitors on efficiency of suppression of proteolytic activation in pneumonia]. 1944 14

Parachlamydia acanthamoebae is an obligate intracellular bacterium that infects free-living amoebae (Acanthamoeba), and is a potential human pathogen associated with hospital-acquired pneumonia. The attachment mechanism of this bacteria to host cells is crucial in bacterial pathogenesis, yet remains undetermined. Hence, we obtained monoclonal antibodies (mAbs) specific to either P. acanthamoebae or amoebae in an attempt to elucidate the attachment mechanism involved. Hybridomas of 954 clones were assessed, and we found that four mAbs (mAb38, mAb300, mAb311, mAb562) that were reactive to the amoebae significantly inhibited bacterial attachment. All mAbs recognized amoebal released molecules, and mAb311 also recognized the amoebal surface. mAbs reacted with the bacteria not only within amoebae, but also when they were released from amoebae (except mAb311). Furthermore, a serine protease inhibitor had an inhibitory effect on the bacterial attachment to amoebae, although none of the mAbs had any synergistic effect on the inhibition of attachment by the protease inhibitor. Taken together, we conclude that concurrent P. acanthoamebae attachment to amoebae is required for several amoebal released molecules and serine protease activity, implying the existence of a complicated host-parasite relationship.
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PMID:A domino-like chlamydial attachment process: concurrent Parachlamydia acanthamoebae attachment to amoebae is required for several amoebal released molecules and serine protease activity. 2240 90


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