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)

Tachyzoites of 2 isolates of Neospora caninum (NC-1 and NC-2) were inoculated subcutaneously (s.c.), intraperitoneally (i.p.), or orally into mice to compare the effects of route of inoculation on pathogenicity. Mice developed more severe disease, and disease occurred sooner when inoculated with the NC-1 isolate compared to the NC-2 isolate. Deaths occurred earlier in mice inoculated i.p. with either isolate. Mice inoculated orally or s.c. with tachyzoites responded similarly to infection. Tissue cysts of the NC-2 isolate produced infections in mice following oral or s.c. inoculation. Lesions seen in mice inoculated with tachyzoites or bradyzoites were primarily acute pneumonia, myositis, encephalitis, ganglioradiculoneuritis, and pancreatitis. In vitro studies demonstrated that tachyzoites of both isolates were killed by incubation in pepsin-HCl solution but not 1% trypsin solution. Bradyzoites of the NC-2 isolate were able to withstand treatment with pepsin-HCl solution.
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PMID:Infections in mice with tachyzoites and bradyzoites of Neospora caninum (Protozoa: Apicomplexa). 211 99

Nine monoclonal antibodies (MAbs) directed to F protein of Sendai virus were obtained and characterized for their protective ability against Sendai virus infection in mice. None of the MAbs showed hemagglutination-inhibition (HI), hemolysis-inhibition (HLI), or neutralization (NT) activities in vitro when assayed by standard methods. Some of the MAbs, however, showed complement-requiring NT (C-NT) and complement-requiring hemolysis (C-HL) activities when assayed in the presence of complement. Passive immunization experiments revealed that the MAbs with higher C-NT and C-HL activities showed protective activity against Sendai virus pneumonia in mice, and that some MAbs with IgG1 isotype having neither C-NT nor C-HL activity also showed the protective activity. Digestion of the MAbs with pepsin which split immunoglobulin molecules into F(ab')2 and Fc fragments greatly suppressed the protective activity. These results suggest that not only complement-mediated immunological responses such as immune virolysis but also antibody-dependent cellular cytotoxicity (ADCC) and/or immune phagocytosis, in which complement system is not necessarily involved, play an important role in the protection of mice from Sendai virus infection.
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PMID:Protection of mice against Sendai virus pneumonia by non-neutralizing anti-F monoclonal antibodies. 216 Oct 73

We describe the production and characterization of three murine monoclonal antibodies (M1-M3) which are directed against different epitopes of the secretory aspartic proteinase of Candida albicans CBS 2730. All antibodies belonged to the IgM class, and they recognized denatured enzyme. Only antibody M1 was capable to react with the active proteinase. Differential reactivity was also observed with a large fragment of the proteinase of C. albicans. All antibodies recognized the corresponding proteinase of C. tropicalis 293 both in the active, and in the denatured state. Denatured porcine pepsin was also recognized by all three antibodies. However, active pepsin was recognized only by antibodies M1 and M2. The antibodies did not inhibit enzymatic activity, and they were not suited for immunofluorescence detection of proteinase on fungal cells. However, employing Western blot analysis, proteinase antigen was detected by antibody M 1 in the serum of a patient suffering from candidal pneumonia. The circulating proteinase antigen was found to be bound to patient's IgM. Implications for the use of monoclonal antibodies in the serodiagnosis of candidosis, and first experiences with other monoclonal anti-proteinase antibodies are discussed.
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PMID:Production and characterization of monoclonal antibodies against secretory proteinase of Candida albicans CBS 2730. 329 31

We present a case of severe pneumonia by Mycoplasma pneumoniae, whose clinical course was complicated by immunodepression, hepatitis and deep venous thrombosis. Treatment with pepsin-treated human immunoglobulins was unsuccessful, whereas prompt recovery was obtained by infusion of human immunoglobulins treated at pH 4.
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PMID:[A severe case of bronchial pneumonia due to Mycoplasma pneumoniae accompanied by immunosuppression, thrombophlebitis and hepatitis resolved with human immunoglobulins]. 383 24

59 patients with suspected or verified septicaemia and 87 patients with suspected or verified bacterial pneumonia were treated with either antibiotics alone or antibiotics combined with a pepsin-treated human gamma globulin (Gamma-Venin). The gamma globulin was given intravenously in repeated doses of 0.15 g/kg body weight. Extensive clinical and laboratory investigations were performed repeatedly in a strictly standardized fashion. Neither the septicaemia group nor the pneumonia group presented significant differences between treated patients and controls for any of the clinical and laboratory variables studied. Hospital stay, duration of fever and symptoms were also unaffected by the gamma globulin treatment. Subdivision of the material according to aetiology provided no additional information. In 9 patients adverse reactions were seen, e.g., shock in 2 individuals.
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PMID:Pepsin-treated human gamma globulin in bacterial infections. A randomized study in patients with septicaemia and pneumonia. 616 28

Microaspiration of contaminated oropharyngeal secretions and gastric contents frequently occurs in intubated critically ill patients, and plays a major role in the pathogenesis of ventilator-associated pneumonia. Risk factors for microaspiration include impossible closure of vocal cords, longitudinal folds in high-volume low-pressure polyvinyl chloride cuffs, and underinflation of tracheal cuff. Zero positive end expiratory pressure, low peak inspiratory pressure, tracheal suctioning, nasogastric tube and enteral nutrition increase the risk for microaspiration. Other patient related factors include supine position, coma, sedation, and hyperglycemia. Technetium 99 labelled enteral feeding is probably the most accurate marker of microaspiration in critically ill patients. However, use of this radioactive marker is restricted to nuclear medicine departments. Blue methylene is a reliable qualitative marker of microaspiration. However, fiberoptic bronchoscopy is required to diagnose microaspiration of blue dye in ICU patients. Quantitative pepsin measurement in tracheal aspirates is accurate in diagnosing microaspiration of gastric contents in critically ill patients. In addition, this marker is easy to use in routine practice. However, pepsin should be detected rapidly after aspiration. In vitro, and clinical studies suggested that semirecumbent position, polyurethane cuffs, positive end expiratory pressure, low-volume low-pressure cuff, and continuous control of cuff pressure were efficient in reducing microaspiration in ICU patients. Other preventive measures such as subglottic aspiration, tapered shape cuff, guayule latex cuff, lateral horizontal patient position, gastrostomy tube, and postpyloric feeding require further investingation.
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PMID:Microaspiration in intubated critically ill patients: diagnosis and prevention. 2167 39

Chronic inflammation induces lymphangiogenesis and blood vessel remodelling. Since aged pneumonia patients often have repeated episodes of aspiration pneumonia, the pathogenesis may involve chronic inflammation. For lymphangiogenesis, VEGFR-3 and its ligand VEGF-C are key factors. No previous studies have examined chronic inflammation or vascular changes in aspiration pneumonia or its mouse models. In lung inflammation, little is known about the effect of blocking VEGFR-3 on lung lymphangiogenesis and, moreover, its effect on the disease condition. This study aimed to establish a mouse model of aspiration pneumonia, examine the presence of chronic inflammation and vascular changes in the model and in patients, and evaluate the effect of inhibiting VEGFR-3 on the lymphangiogenesis and disease condition in this model. To induce aspiration pneumonia, we repeated inoculation of pepsin at low pH and LPS into mice for 21-28 days, durations in which bronchioalveolar lavage and plasma leakage in the lung suggested the presence of exaggerated inflammation. Conventional and immunohistochemical analysis of tracheal whole mounts suggested the presence of chronic inflammation, lymphangiogenesis, and blood vessel remodelling in the model. Quantitative RT-PCR of the trachea and lung suggested the involvement of lymphangiogenic factor VEGF-C, VEGFR-3, and pro-inflammatory cytokines. In the lung, the aspiration model showed the presence of chronic inflammation and exaggerated lymphangiogenesis. Treatment with the VEGFR inhibitor axitinib or the VEGFR-3 specific inhibitor SAR131675 impaired lymphangiogenesis in the lung and improved oxygen saturation in the aspiration model. Since the lung is the main site of aspiration pneumonia, the changes were intensive in the lung and mild in the trachea. Human lung samples also showed the presence of chronic inflammation and exaggerated lymphangiogenesis, suggesting the relevance of the model to the disease. These results suggest lymphatics in the lung as a new target of analysis and therapy in aspiration pneumonia.
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PMID:Chronic inflammation, lymphangiogenesis, and effect of an anti-VEGFR therapy in a mouse model and in human patients with aspiration pneumonia. 2534 79