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

Three cell wall-derived Pseudomonas aeruginosa vaccines were evaluated for their capacity to provide protection from experimental pseudomonas pneumonia in guinea pigs. Two vaccines, Pseudogen, a heptavalent lipopolysaccharide vaccine, and PEV-01, a polyvalent glycine-EDTA cell wall extract, each produced hemagglutinating, opsonic, and serum bactericidal antibodies in guinea pigs. Significant protection from fatal hemorrhagic pneumonia was conferred by vaccination with these products. Purified, high-molecular weight polysaccharide vaccine was a less potent immunogen in guinea pigs and provided less protection from pneumonia. Protection from fatal pneumonia in vaccinees correlated with more rapid clearance of viable P. aeruginosa from lung tissue during the first 6 hr of infection. It appears that active immunization with certain cell wall-derived pseudomonas antigens can provide protection against experimental pseudomonas pneumonia.
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PMID:Efficacy of cell wall Pseudomonas aeruginosa vaccines for protection against experimental pneumonia. 641 11

Pneumonia due to Pseudomonas aeruginosa is associated with unusually high mortalities. Accordingly, efforts to define better the most important components of lung defenses against this infection are justified as a prelude to defining improved management strategies. In this report, a guinea pig model of experimental aspiration pseudomonas pneumonia was employed for studies of cellular and humoral mechanisms of pulmonary defense. Animals treated with cortisone acetate plus cyclophosphamide experienced decreased survival from pneumonia, and survival rates correlated directly with the degree of myelosuppression. Numbers of pulmonary macrophages and polymorphonuclear neutrophils were reduced in drug-treated animals before impairment of macrophage antibacterial function. Thus, a reduction in numbers of phagocytes alone was sufficient to markedly reduce lung defenses. In additional experiments, normal guinea pigs were vaccinated with a lipopolysaccharide pseudomonas vaccine. Improved survival from pneumonia correlated with high titers of type-specific, heat-stable opsonic antibody. It is concluded that adequate numbers of lung phagocytes, plus type-specific opsonic antibody, represent the ideal status for lung defense against P. aeruginosa infection.
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PMID:Host defense mechanisms against pneumonia due to Pseudomonas aeruginosa. 644 67

C3H mice develop heavier degrees of Pneumocystis carinii pneumonia than other mouse strains tested. We have compared P. carinii pneumonia in two strains of C3H mice: C3H/HeJ mice, which are unresponsive to the effects of bacterial lipopolysaccharide (LPS), have defects in macrophage function, and have increased antibody responses to orally administered T-dependent antigens; and C3HeB/FeJ mice, which are immunologically normal. P. carinii pneumonia was induced by corticosteroids, and the intensity of the infection was judged by a semiquantitative histopathologic scoring system. Heavier degrees of infection were found in C3H/HeJ mice than in C3HeB/FeJ mice. Serum antibodies to P. carinii, measured by an indirect fluorescent antibody technique, were mainly of the IgG class in both strains of mice and varied inversely with the intensity of P. carinii infection in the lungs. Antibody levels were significantly higher in C3H/HeJ mice than in C3HeB/FeJ mice. These data suggest that C3H/HeJ have increased susceptibility to the effects of steroids of host defenses against P. carinii, and heightened serum antibody responses to the organism.
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PMID:Experimental Pneumocystis carinii pneumonia in C3H/HeJ and C3HeB/FeJ mice. 660 Nov 89

Recent studies in guinea pigs indicated that active vaccination with a cell wall-derived, lipopolysaccharide (LPS) pseudomonas vaccine confers specific protection against acute pneumonia. This study analyzed the immune mechanisms by which LPS pseudomonas vaccine offers local protection to the lung. Neither parenteral vaccination nor direct exposure of lung tissues to living Pseudomonas activated alveolar macrophages. However, serum opsonic activity that specifically enhanced phagocytosis of Pseudomonas by alveolar macrophages was significantly increased (P < 0.05) in vaccinated animals. Serum pseudomonas opsonins were heat-stable but were sensitive to reduction of macroglobulins by 2-mercaptoethanol. Within 3 hr after establishment of experimental pseudomonas pneumonia, a fourfold increase in local pseudomonas opsonins was found in bronchial fluids from vaccinated animals, presumably secondary to diffusion of serum proteins into local inflammatory fluids. Thus, Pseudomonas-specific opsonic antibody appears necessary to augment alveolar macrophage phagocytosis after LPS vaccination, and local vaccination of the respiratory tract is not required to provide adequate local pseudomonas opsonins during acute pneumonia.
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PMID:Mechanism for pulmonary protection by lipopolysaccharide pseudomonas vaccine. 677 32

Chronic respiratory infection with Pseudomonas aeruginosa is a leading clinical problem among patients with cystic fibrosis. Because antimicrobial agents are usually ineffective in eradicating these infections, additional therapeutic or prophylactic measures should be considered. In this study, an experimental guinea pig model of chronic Pseudomonas aeruginosa bronchopneumonia was utilized to determine whether active immunization with lipopolysaccharide (LPS) P. aeruginosa antigen may favorably influence the course of this infection. Experimental pneumonia was established by tracheobronchial instillation of suspensions of microscopic agar beads, which were impregnated with viable P. aeruginosa. After 4 wk of infection, the geometric mean (reciprocal) passive hemagglutinating Pseudomonas antibody titer was 185+/-1.3, and lungs contained 16.8+/-4 x 10(3) colony-forming units Pseudomonas/ml of lung homogenate. Pseudomonas immunization, given prior to a 4-wk infection, resulted in significantly higher passive hemagglutinating titers (474+/-1.4; P < 0.05), lower numbers of viable Pseudomonas in lung tissues (2.4+/-0.6 x 10(3); P < 0.01), and reduced histopathology in lungs. In contrast, providing Pseudomonas immunization to animals 2 wk after pulmonary infection was established, offered no apparent benefit. Likewise, no protection was afforded by prophylactic immunization with a non-Pseudomonas LPS antigen (Escherichia coli J5 vaccine). Using a Raji cell assay, modified to detect circulating immune complexes in vaccinated and infected guinea pig sera, there was no evidence that active immunization increased the frequency of circulating immune complexes in infected guinea pigs. It is concluded that prophylactic immunization with Pseudomonas LPS antigen may confer protection from subsequent Pseudomonas bronchopneumonia, but that immunization during established infection is not beneficial.
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PMID:Active immunization with lipopolysaccharide Pseudomonas antigen for chronic Pseudomonas bronchopneumonia in guinea pigs. 679 29

Groups of guinea pigs received four injections intramuscularly of lipopolysaccharide vaccine derived from Pseudomonas aeruginosa, cross-protective core glycolipid vaccine derived from the J-5 mutant of Escherichia coli O111, or saline during a two-week period. Titers of passive hemagglutinating antibody to vaccine antigens in serum routinely increased fourfold or more. Experimental hemorrhagic pseudomonas pneumonia was then induced, from which the rates of survival were 15% among animals receiving saline, 81% among animals receiving pseudomonas vaccine (P less than 0.001), and 42% among animals receiving J-5 vaccine. Thus, only weak cross-protection against pseudomonas pneumonia was detected in the recipients of J-5 vaccine. Further studies revealed no protection against pneumonia due to either E. coli or Klebsiella in animals receiving J-5 vaccine. From these data, species-specific vaccination appears to be superior to vaccination with cross-protective antigen against experimental pseudomonas pneumonia.
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PMID:Type-specific vs. cross-protective vaccination for gram-negative bacterial pneumonia. 679 87

Epizootics of pneumonia in mink caused by Pseudomonas aeruginosa were investigated to characterize the serotype of organisms and to identify possible predisposing factors. Most epizootics were associated with P aeruginosa Fisher serotype 1, and a few were associated with 3 other serotypes. There were no predisposing factors identified that could be used to differentiate farms affected and those not affected with pseudomonas pneumonia. Cultural studies indicated that P aeruginosa was present in mink from affected and nonaffected herds. Organisms isolated included serotypes associated with naturally occurring disease. Serostudy results were similar among herds. A prospective field vaccination trial did not yield definitive results, since only slight losses occurred in both vaccinated and nonvaccinated mink. Significant levels of antibody were detected in mink 15 to 17 weeks after they were given a single dose of P aeruginosa lipopolysaccharide vaccine.
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PMID:Field studies: pseudomonas pneumonia of mink. 680 21

Pneumocystic carinii pneumonia, which is a major cause of death among patients suffering from acquired immunodeficiency syndrome, has often been treated successfully with pentamidine isethionate. This study examines pentamidine effects on cellular and secreted proteins from rat alveolar macrophages by two-dimensional gel electrophoresis and computerized image analysis. Over 100 secreted proteins were detected by fluorography. Fluorography showed pentamidine diminished tumor necrosis factor and interleukin-1 release along with other proteins. Effects of combined bacterial lipopolysaccharide and pentamidine were more pronounced on secreted versus cellular proteins in protein amount and pattern difference. Thus pentamidine exhibited a general repressive effect on cellular and secreted protein expression in resting and activated macrophages.
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PMID:Gel electrophoretic analysis of cellular and secreted proteins from resting and activated rat alveolar macrophages treated with pentamidine isethionate. 758 50

We examined the kinetics of tumor necrosis factor (TNF) production induced by Escherichia coli lipopolysaccharide (LPS) in relation to LPS tolerance and endotoxemic lesions of piglets. The plasma of piglets demonstrated cytotoxicity to TNF-sensitive L929 cells between 0.5 and 4 h after inoculation with 200 micrograms kg-1 of LPS. This cytotoxicity was neutralized by anti-bovine TNF serum. These piglets had disseminated intravascular coagulation (DIC) and meningoencephalitis. However, if piglets were first treated with three doses of 40 micrograms kg-1 of LPS, both TNF production and the occurrence of DIC were inhibited when 200 micrograms kg-1 of LPS was inoculated into these piglets. Repetitive inoculation with increasing doses of LPS induced fibrinoid vasculitis, meningoencephalitis and pneumonitis, while hemorrhage was minimal. A very low amount of TNF activity was detected from most of the samples of a piglet after repeated LPS inoculation. These results suggested that severity of the hemorrhagic and thrombotic lesions might relate to the amount of endogenous TNF activity, and that LPS tolerance might relate to inhibition of TNF production.
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PMID:Endogenous tumor necrosis factor (TNF) production and modification of pathological lesions in experimental Escherichia coli endotoxemia of piglets. 760 37

A murine pulmonary model was used to study the mucosal immune response to Shigella flexneri serotype 2a infection. Inoculation of BALB/cJ mice with shigellae via the intranasal route resulted in bacterial invasion of bronchial and alveolar epithelia with concomitant development of acute suppurative bronchiolitis and subsequent development of lethal pneumonia. The pathology of pulmonary lesions resembled the colitis that characterizes shigellosis in humans and primates. Significant protection against a lethal dose of S. flexneri 2a was observed in mice previously infected with two sublethal doses of the homologous strain. Immunity against lethal challenge was associated with decreased bacterial invasion of the mucosal epithelium. Over the course of two sublethal challenges, which constituted primary and secondary immunizations, mice developed pulmonary and serum immunoglobulin G and A antibody recognizing both lipopolysaccharide and invasion plasmid antigens IpaB and IpaC. Immune mice and naive control mice differed in lung lavage cytokine levels following lethal challenge. Immune mice developed significantly elevated levels of pulmonary gamma interferon within 6 h of challenge, while naive control mice developed elevated levels of this cytokine later during the initial 24-h period. Both groups had elevated levels of gamma interferon during the 24- to 48-h period of infection. Both groups also had elevated levels of tumor necrosis factor alpha within 6 h of challenge, but the control mice had significantly higher levels at the 48- and 72-h time points. Elevated levels of interleukin-4 were observed only in immunized mice. This cytokine appeared within 24 h and receded between 48 and 72 h. Fluorescence-activated cell sorter analysis of lung parenchymal cells showed that both groups experienced an initial influx of monocytes, but the proportion of this cell type began to recede in immunized mice after 48 h of infection, while peak levels were maintained in the control animals. These studies suggest that elements of local B lymphocyte activity, as well as Th1 and Th2 lymphocyte activity, may contribute to the survival of immune mice after intranasal challenge with shigellae.
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PMID:Antibody and cytokine responses in a mouse pulmonary model of Shigella flexneri serotype 2a infection. 772 7


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