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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enzyme-linked immunosorbent assay (ELISA) for detecting antibody to Mycoplasma hyopneumoniae in porcine serum is described. The results are presented as an ELISA ratio, calculated by dividing the absorbance of the test sample by the mean absorbance of control negative sera. In known infected pigs, the ELISA ratio was highest when the serum concentration applied to the ELISA plate was diluted 1 in 20 in PBS - Tween. Mean ELISA ratios ranged from 1.2 +/- 0.3 for pigs without porcine enzootic pneumonia (PEP) lesions to 5.5 +/- 1.5 for pigs observed with a PEP lesion reacting positively with immunofluorescent histopathology. Pigs observed with typical PEP lesions at slaughter, but not confirmed by immunofluorescent histopathology had a mean ELISA ratio of 4.9 +/- 1.7. The ELISA was highly sensitive (95.6%) and specific (98.8%) when pig sera from commercial piggeries of known M hyopneumoniae infection status were assessed. No cross-reactivity with serum from a pig hyperimmunised with killed M flocculare was detected, and reactivity with serum from another pig hyperimmunised with killed M hyorhinis showed only weak cross-reactivity, which failed to reach the ELISA positive threshold (ELISA ratio 3) for M hyopneumoniae.
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PMID:Evaluation of an enzyme-linked immunosorbent assay for the detection of Mycoplasma hyopneumoniae antibody in porcine serum. 144 72

Three experiments were performed to evaluate the inflammatory response, the antibody response and protection from experimental challenge of various Actinobacillus pleuropneumoniae serotype 5 (Ap5) vaccines in swine. In the first experiment, subcutaneous injections of either a water-in-oil (W/O) emulsion or Freund's complete adjuvant (FCA) caused lesions at the site of injection, while intraperitoneal injection of the W/O emulsion caused no lesions. In the second experiment, intraperitoneal (IP) injection of a W/O emulsion containing unwashed Ap5 cells (6-h culture) and/or supernates from a 24-h culture resulted in severe peritoneal lesions, while W/O emulsion containing PBS-washed Ap5 cells resulted in minimal peritoneal lesions. Ap5 alone or W/O alone failed to cause peritoneal lesions. The third experiment compared the antibody response and protection from challenge of pigs immunized with either 6-h PBS-washed Ap5 cells emulsified in oil - IP, 6-hour Ap5 cells adjuvanted with dimethyl diodacyl ammonium bromide - IP, Ap5 antigen alone - IP, a commercial vaccine - subcutaneously or saline - IP. All groups, except the saline-treated group, responded with high antibody titers to Ap5 2 weeks following vaccination; however, titers from the W/O plus antigen group were significantly higher than the three other groups (P less than 0.05). Following intranasal challenge with Ap5, all animals responded with increased antibody titers. All pigs were euthanized 10 days after challenge and evaluated for pneumonia and the lungs cultured for bacteria. The lungs of all pigs, excepting the W/O plus antigen group, contained pneumonic lesions and A. pleuropneumoniae was cultured from these lesions. These results, along with results from other groups, suggest that intraperitoneal immunization using oil-adjuvanted vaccine may be an effective method for protecting pigs from pneumonia due to A. pleuropneumoniae. Its efficacy may be due to stimulation of local respiratory mucosal immunity.
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PMID:Comparison of protective immunity and inflammatory responses of pigs following immunization with different Actinobacillus pleuropneumoniae preparations with and without adjuvants. 281 78

An experimental model of hypersensitivity pneumonitis is presented. New Zealand white rabbits, previously immunized against yeast-derived zymosan, reacted to intratracheal challenge developing extensive pneumonitis. The lesions healed in a few weeks. Control animals challenged with inert particulate material (latex beads) or suspending fluid (PBS-Mg++) did not show pulmonary inflammation. Nonimmunized rabbits developed only transient pneumonitis after zymosan challenge. This reaction was clearly different from that seen in the group of immunized animals. The model reveals that biologically active substances such as zymosan, which is able to activate the alternate pathway of complement and mononuclear phagocytes, requires an active immune state in order to cause significant tissue damage. Isolated exposure to this kind of substance may not be sufficient to cause lung disease.
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PMID:Zymosan-induced experimental hypersensitivity pneumonitis in rabbits. 738 1

Intranasal Herpes simplex virus type 1 (HSV-1) infection of mice caused pneumonia. Manifestations of the disease included: histological pneumonitis, pulmonary influx of lymphocytes, decreased pulmonary compliance, and decreased survival. Immunohistochemical staining demonstrated iNOS induction and the nitrotyrosine antigen in the lungs of infected, but not uninfected mice, suggesting that nitric oxide contributes to the development of pneumonia. To elucidate the role of nitric oxide in the pathogenesis of HSV-1 pneumonia, infected mice were treated either with the inhibitor of nitric oxide synthase activity, N(G)-monomethyl-L-arginine (L-NMMA), or, as a control, with PBS or D-NMMA. L-NMMA treatment decreased the histological evidence of pneumonia and reduced the bronchoalveolar lavage lymphocyte number to one-quarter of the total measured in control-treated mice. L-NMMA treatment significantly improved survival and pulmonary compliance of HSV-1-infected mice. Strikingly, the L-NMMA-mediated suppression of pneumonia occurred despite the presence of a 17-fold higher pulmonary viral titer. Taken together, these data demonstrated a previously unrecognized role of nitric oxide in HSV-1-induced pneumonia. Of note, suppression of pneumonia occurred despite higher pulmonary virus content; therefore, our data suggest that HSV-1 pneumonia is due to aspects of the inflammatory response rather than to direct viral cytopathic effects.
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PMID:Suppression of herpes simplex virus type 1 (HSV-1)-induced pneumonia in mice by inhibition of inducible nitric oxide synthase (iNOS, NOS2). 915 90

We performed an open, prospective, randomized clinical trial in 51 patients receiving mechanical ventilation for more than 72 h, in order to evaluate the impact of using either invasive (protected specimen brush [PSB] and bronchoalveolar lavage [BAL] via fiberoptic bronchoscopy) or noninvasive (quantitative endotracheal aspirates [QEA]) diagnostic methods on the morbidity and mortality of ventilator-associated pneumonia (VAP). Patients were randomly assigned to two groups: Group A patients (n = 24) underwent QEA, PSB, and BAL; Group B patients (n = 27) underwent only QEA cultures. Empiric antibiotic treatment was given according to the attending physician and was modified according to the results of cultures and sensitivity in Group A using PSB and BAL results and in Group B based upon QEA cultures. Bacteriologic cultures were done quantitatively for EA, PSB, and BAL. Thresholds of > or = 10(5), > or = 10(3), and > or = 10(4) CFU/ml were used for QEA, PSB, and BAL, respectively. Microbial cultures from Group A patients were positive in 16 (67%) BAL samples, 14 (58%) PSB samples, and 16 (67%) QEA samples. In Group B patients, QEA microbial cultures yielded positive results in 20 of 27 (74%) samples. In Group A, there was total agreement between culture results of the three techniques on 17 (71%) occasions. In five (21%) cases, QEA coincided with either BAL or PBS. In only two (8%) cases, QEA cultures did not coincide with either PSB or BAL. No cases of positive BAL or PSB cultures had negative QEA cultures. Initial antibiotic treatment was modified in 10 (42%) patients from Group A and in four (16%) patients from Group B (p < 0.05). The observed crude mortality rate was 11 of 24 (46%) in Group A, and 7 of 27 (26%) in Group B, whereas the adjusted mortality rates (observed crude minus predicted at admission) for Groups A and B were 29 and 10%, respectively. There were no statistically significant differences when comparing crude and adjusted mortality rates of Groups A and B. There were no differences in mortality between both groups when comparing pneumonia, considering together Pseudomonas aeruginosa and Acinetobacter spp. (Group A, 33% versus Group B, 27%). There were no differences between Groups A and B with regard to ICU stay duration and total duration of mechanical ventilation. In this pilot study, the impact of bronchoscopy was to lead to more frequent antibiotic changes with no change in mortality. Further studies with larger population samples are warranted to confirm these findings.
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PMID:Impact of invasive and noninvasive quantitative culture sampling on outcome of ventilator-associated pneumonia: a pilot study. 947 43

An ultrastructural and histological study was made to analyse the structural and cellular features of the pulmonary lesions produced in Wistar rats by intraperitoneal (i.p.) administration of cyclophosphamide (two i.p. doses of 150 mg CP/1 kg bw/1 ml PBS). Rats exposed to cyclophosphamide (CP) developed a condition whose morphological picture corresponded to endogenous lipid pneumonia and/or pulmonary alveolar proteinosis-like changes. Damage to the endothelium and neutrophil accumulation in lung vascular bed were found to be potential initiators of endogenous lipid pneumonia-type changes. The possibility of the evolution of the acute lung injury into endogenous lipid pneumonia-type changes and into alveolar proteinosis-like changes was demonstrated. The results of the study supplement the existing theories of pulmonary alveolar proteinosis pathogenesis.
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PMID:Alveolar cells in cyclophosphamide-induced lung injury. II. Pathogenesis of experimental endogenous lipid pneumonia. 1050 30

Secondary pneumococcal pneumonia is a serious complication during and shortly after influenza infection. We established a mouse model to study postinfluenza pneumococcal pneumonia and evaluated the role of IL-10 in host defense against Streptococcus pneumoniae after recovery from influenza infection. C57BL/6 mice were intranasally inoculated with 10 median tissue culture infective doses of influenza A (A/PR/8/34) or PBS (control) on day 0. By day 14 mice had regained their normal body weight and had cleared influenza virus from the lungs, as determined by real-time quantitative PCR. On day 14 after viral infection, mice received 10(4) CFU of S. pneumoniae (serotype 3) intranasally. Mice recovered from influenza infection were highly susceptible to subsequent pneumococcal pneumonia, as reflected by a 100% lethality on day 3 after bacterial infection, whereas control mice showed 17% lethality on day 3 and 83% lethality on day 6 after pneumococcal infection. Furthermore, 1000-fold higher bacterial counts at 48 h after infection with S. pneumoniae and, particularly, 50-fold higher pulmonary levels of IL-10 were observed in influenza-recovered mice than in control mice. Treatment with an anti-IL-10 mAb 1 h before bacterial inoculation resulted in reduced bacterial outgrowth and markedly reduced lethality during secondary bacterial pneumonia compared with those in IgG1 control mice. In conclusion, mild self-limiting influenza A infection renders normal immunocompetent mice highly susceptible to pneumococcal pneumonia. This increased susceptibility to secondary bacterial pneumonia is at least in part caused by excessive IL-10 production and reduced neutrophil function in the lungs.
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PMID:IL-10 is an important mediator of the enhanced susceptibility to pneumococcal pneumonia after influenza infection. 1518 40

The He-Ne-laser induced effects in human blood leukocytes in the presence of autologic plasma were investigated. Experiments were performed in two ways: (1) He-Ne-laser irradiation of cells in the presence of autologic plasma or (2) laser irradiation and subsequent addition of autologic plasma to the cell suspension. The concentration dependencies of plasma additions were evaluated. To obtain different concentrations of porphyrins in plasma samples, we either diluted the samples with PBS or selected patients with different porphyrin plasma content. The effects of He-Ne-laser irradiation were characterized by the maximum effect dose (Dmax) of irradiation and the degree of maximum cell activation (Amax, priming index). In the first series of experiments, we irradiated leukocytes in the presence of autologic plasma taken from patients with pneumonia and bronchial asthma. It was found that Dmax decreased with increasing porphyrin concentration in plasma. It was observed that, at low porphyrin concentrations, Amax increased severalfold with increasing photosensitizer concentration. At a porphyrin concentration of 0.46 pmol a decrease in Amax was detected as the porhyrin concentration increased. The same effects were revealed at high doses of laser irradiation. Very similar effects were found in experiments with the addition of irradiated plasma to cells. However, the Amax value was considerably less compared to that after irradiation in the presence of plasma (160% vs. 230 - 270% upon combined irradiation of cells and plasma). The Dmax value was higher in the series of experiments in which plasma was irradiated separately. The results suggest that laser-induced leukocyte activation can be mediated by blood plasma porphyrins and the products of lipid peroxidation formed as a result of porphyrin-photosensitized lipid oxidation.
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PMID:[The role of blood plasma porphyrins in the effects of He-Ne-laser on human leukocytes]. 1621 65

Surface-expressed bacterial polysaccharides are often immunodominant, protective antigens. However, these antigens are chemically and serologically highly heterogeneous, and conjugation to protein carriers is often necessary to enhance their immunogenicity. Here we show the efficacy of intranasal immunization of mice with attenuated Salmonella enterica serovar Typhimurium expressing the O antigen portion of Pseudomonas aeruginosa lipopolysaccharide. P. aeruginosa is an ideal model system because it can cause a myriad of localized and systemic infections. In particular, this bacterium is a leading cause of hospital-acquired pneumonia and is responsible for infections after burns and after eye injury. In addition, there are mouse models of infection that mimic the clinical manifestations of P. aeruginosa infections. Immunized mice were highly protected against infection, with long-lasting immunity to acute P. aeruginosa pneumonia, whereas mice immunized with Salmonella containing only the cloning vector or PBS were not. Prophylactic and therapeutic administration of sera from vaccinated animals protected naive mice. Intranasal vaccination also provided complete protection from infections after burns and reduced pathology after corneal abrasions. These results indicate that intranasal delivery of heterologously expressed polysaccharide antigens provides protection at distinct sites of infection. This approach for the expression and delivery of polysaccharide antigens as recombinant immunogens could be easily adapted to develop vaccines for many infectious agents, without the need for complicated purification and conjugation procedures.
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PMID:Intranasal immunization with heterologously expressed polysaccharide protects against multiple Pseudomonas aeruginosa infections. 1736 May 74

The pathogenesis and optimal treatments for severe acute respiratory syndrome (SARS) are unclear, although corticosteroids were used to reduce lung and systemic inflammation. Because the pulmonary pathology of porcine respiratory coronavirus (PRCV) in pigs resembles SARS, we used PRCV as a model to clarify the effects of the corticosteroid dexamethasone (DEX) on coronavirus (CoV)-induced pneumonia. Conventional weaned pigs (n = 130) in one of four groups (PRCV/phosphate-buffered saline [PBS] [n = 41], PRCV/DEX [n = 41], mock/PBS [n = 23], and mock/DEX [n = 25]) were inoculated intranasally and intratracheally with the ISU-1 strain of PRCV (1 x 10(7) PFU) or cell culture medium. DEX was administered (once daily, 2 mg/kg of body weight/day, intramuscularly) from postinoculation day (PID) 1 to 6. In PRCV/DEX pigs, significantly milder pneumonia, fewer PRCV-positive cells, and lower viral RNA titers were present in lungs early at PID 2; however, at PID 4, 10, and 21, severe bronchointerstitial pneumonia, significantly higher numbers of PRCV-positive cells, and higher viral RNA titers were observed compared to results for PRCV/PBS pigs. Significantly lower numbers of CD2(+), CD3(+), CD4(+), and CD8(+) T cells were also observed in lungs of PRCV/DEX pigs than in those of PRCV/PBS pigs at PID 8 and 10, coincident with fewer gamma interferon (IFN-gamma)-secreting cells in the tracheobronchial lymph nodes as determined by enzyme-linked immunospot assay. Our results confirm that DEX treatment alleviates PRCV pneumonia early (PID 2) in the infection but continued use through PID 6 exacerbates later stages of infection (PID 4, 10, and 21), possibly by decreasing cellular immune responses in the lungs (IFN-gamma-secreting T cells), thereby creating an environment for more-extensive viral replication. These data have potential implications for corticosteroid use with SARS-CoV patients and suggest a precaution against prolonged use based on their unproven efficacy in humans, including possible detrimental secondary effects.
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PMID:Altered pathogenesis of porcine respiratory coronavirus in pigs due to immunosuppressive effects of dexamethasone: implications for corticosteroid use in treatment of severe acute respiratory syndrome coronavirus. 1794 63


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