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

The objective of this study was to characterize the humoral immune response to chlamydial genital infection of mice with the mouse pneumonitis agent (MoPn). With an enzyme-linked immunoabsorbent assay, immunoglobulin G antibodies to MoPn were first detected in plasma by day 14. Peak plasma antibody concentrations were reached by day 49, and this response did not decline significantly throughout the 300-day monitoring period. Immunoglobulin A against MoPn could first be detected in pooled vaginal washes by day 21 after infection and had reached peak concentrations by day 28, but anti-MoPn immunoglobulin G was not consistently present in secretions. The antibody response in secretions had declined slightly by day 300. Immunoblot analysis revealed that the early phase of the plasma antibody response to MoPn as a result of genital infection was against lipopolysaccharide, the major outer membrane protein, and a 62-kilodalton (kDa) protein. In secretions, early-phase immunoglobulin A antibodies were directed to the major outer membrane protein and lipopolysaccharide. Late reactions to 15-, 22-, and 83-kDa proteins in plasma were noted. Late reactions to the 62-kDa protein in secretions were also noted. The cause of these late responses remains unexplained. When mice were challenged intravaginally with MoPn at 50-day intervals after the primary infection, it was found that mice inoculated on day 100 or after were susceptible to reinfection. Susceptibility could not be related to a decline in the antibody concentration in plasma or secretions or in the antibody response to specific components of MoPn as measured by immunoblot analysis.
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PMID:Humoral immune response to chlamydial genital infection of mice with the agent of mouse pneumonitis. 274 54

A human IgM monoclonal antibody (MA-1C1) to Fisher immunotype 3 Pseudomonas aeruginosa lipopolysaccharide antigen was evaluated for in vivo activity in a guinea pig model of experimental pneumonia. Pharmacokinetics of MA-1C1 were compared in infected and noninfected animals. Intravenous bolus infusion of MA-1C1, 1 mg/kg, resulted in peak serum antibody concentrations of 3.8 +/- 0.08 and 3.7 +/- 0.05 micrograms/ml in infected and noninfected animals, respectively. Serum half-lives were 25 and 22 h in infected and noninfected groups. Treatment with a single intravenous infusion of MA-1C1 improved survival from pneumonia and was effective over a broad dose range (0.1-2.5 mg/kg). Cumulative survivals were 18 of 47 in the MA-1C1 group and 0 of 31 in controls (P less than .001). Treatment with MA-1C1 also resulted in fewer positive blood cultures 12 h after infection (P = .04). Although MA-1C1 penetrated into inflamed bronchial fluids, local concentrations were only 5% of the concentrations achieved in serum. Thus, MA-1C1 seems to provide significant therapeutic activity against experimental P. aeruginosa pneumonia by preventing dissemination of infection from the lung.
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PMID:Treatment of experimental Pseudomonas aeruginosa pneumonia with a human IgM monoclonal antibody. 276 Apr 99

Interleukin-1 (IL-1) release by alveolar macrophages (AMs) from 29 patients with primary bronchogenic carcinoma, lung metastases, acute pneumonitis, and chronic infection was evaluated in response to a standard stimulus, lipopolysaccharide (LPS). The results were compared to those of AMs from normal smokers or nonsmokers (volunteers). AMs derived from healthy smokers secreted significantly more IL-1 than AMs from nonsmokers. In contrast, AMs from smokers affected with primary lung cancer have lost their capacity of secreting high levels of IL-1, whereas IL-1 secretion was high in nonsmokers with hematogenous metastases. AMs release high IL-1 levels in patients with acute bacterial infections. A significant correlation exists between numbers of AMs and IL-1 levels in normal individuals, a relationship which disappears in patients. These observations suggest that AMs in inflammatory lung disease, even discrete, have an increased capacity to secrete IL-1 on stimulation with LPS. They also suggest that an intrinsic dysfunction of AMs may accompany primary bronchogenic carcinoma. The influence of tobacco in modifying the functions of AMs is stressed.
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PMID:Interleukin-1 secretion by lipopolysaccharide-stimulated alveolar macrophages. Relationships to cell numbers--influence of smoking habits. 281 73

Following infection of mice with larvae of the canine roundworm Toxocara canis, there is a persistent pneumonitis. Heretofore, nothing was known about the immunologic potential of the cells that constitute this inflammatory exudate. By performing bronchoalveolar lavage (BAL), enough inflammatory cells were obtained to compare the local pulmonary immune response to T. canis infection with the systemic immune response as reflected in the peripheral blood and spleen cells of the same mice. Groups of C57BL/6J female mice were given 100 infective ova and BAL, peripheral blood, and spleen cells collected on days 8, 11, 14, and 17 postinfection. The percentage of eosinophils in the BAL averaged about 80% and was four to five times as great as that in the peripheral blood at all times assayed. Use of concanavalin A (ConA)-elicited lymphocyte blastogenesis to evaluate T-lymphocyte activity revealed that BAL T-cell activity was low on day 8 and peaked on day 11. When the B-cell mitogen lipopolysaccharide was used in the assay, there appeared to be far less BAL cell reactivity compared with BAL T-cell activity. Both B- and T-cell responses of the BAL cells were only a fraction of the responses seen concurrently in spleen cells. Use of Toxocara exoantigens in the blastogenesis assay revealed that Toxocara exoantigens could elicit between 20 and 95% of the ConA response in BAL cells, while in spleen cells Toxocara exoantigens could only elicit 1 to 5% of the ConA response. These results suggest that BAL is a useful method for recovering local inflammatory cells that possess detectable immunologic activity. In the case of pulmonary toxocariasis, eosinophils account for the majority of the cells that are present, with most of the remaining cells being T. canis antigen-specific T lymphocytes.
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PMID:Use of bronchoalveolar lavage to compare local pulmonary immunity with the systemic immune response of Toxocara canis-infected mice. 288 14

The unusually high mortality associated with Pseudomonas aeruginosa pneumonia has provided an incentive for the development of immunologic strategies for preventing or treating this infection. A guinea pig model of experimental P. aeruginosa pneumonia was employed to determine prophylactic efficacy of active immunization with a detoxified lipopolysaccharide vaccine; efficacy of passive immune therapy utilizing a new hyperimmune immunoglobulin G preparation enriched for antibodies to P. aeruginosa immunotypes 1, 2, 4, and 6; and efficacy of active and passive immunization against the mucoid exopolysaccharide antigen associated with mucoid strains of P. aeruginosa. Each of these immunologic methods provided an element of protection against P. aeruginosa pneumonia.
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PMID:Active and passive immunization strategies for Pseudomonas aeruginosa pneumonia. 294 9

A human immunoglobulin G preparation, enriched in antibodies to lipopolysaccharide (LPS) Pseudomonas aeruginosa antigens (PA-IGIV) and murine monoclonal antibodies (MAb) to P. aeruginosa Fisher immunotype-1 (IT-1) LPS antigen and outer membrane protein F (porin), were evaluated for therapeutic efficacy in a guinea pig model of P. aeruginosa pneumonia. The concentration of antibodies to IT-1 LPS was 7.6 micrograms/ml in PA-IGIV and 478 micrograms/ml in the IT-1 MAb preparation. No antibody to IT-1 was detected in MAb to porin. For study, animals were infected by intratracheal instillation of IT-1 P. aeruginosa and then treated 2 h later with intravenous infusions of PA-IGIV, IT-1 MAb, or porin MAb. Control groups received intravenous albumin, and routinely died from pneumonia. Both PA-IGIV (500 mg/kg) and IT-1 MAb (greater than or equal to 2.5 mg/kg) treatment resulted in increased survival (P less than 0.01 to 0.001), and also improved intrapulmonary killing of bacteria. Porin MAb failed to protect from fatal pneumonia. IT-1 MAb treatment produced more survivals than did PA-IGIV treatment but only at dosages of MAb resulting in serum antibody concentrations greater than those achieved with PA-IGIV. PA-IGIV and IT-1 MAb demonstrated in vitro and in vivo (posttreatment guinea pig serum) opsonophagocytic activity for the IT-1 challenge strain. However, the polyclonal preparation required complement, whereas the MAb did not. We conclude that passive immunization with polyclonal hyperimmune P. aeruginosa globulin or with MAb to LPS antigens may be useful in the treatment of acute P. aeruginosa pneumonia. The relative efficacies of such preparations may be limited, however, by their type-specific LPS antibody concentrations.
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PMID:Polyclonal and monoclonal antibody therapy for experimental Pseudomonas aeruginosa pneumonia. 309 85

Three immunoglobulin preparations for intravenous infusion were compared in vivo to determine their relative protective capacity against several gram-negative and gram-positive pathogens. Polyglobin N is a conventional IgG concentrate. Psomaglobin N is identical in formulation to Polyglobin N but is prepared from the plasma of donors who have naturally high levels of antibody to lipopolysaccharide antigens of Pseudomonas aeruginosa. IgGMA is a conventional IgG concentrate containing 12% IgG and 16% IgA. In a murine model of burn wound sepsis the three IgG preparations were similarly protective against three or ten strains of P. aeruginosa. Psomaglobin N and Polyglobin N were significantly (p less than or equal to 0.015) more protective than IgGMA against six of ten and three of ten strains of P. aeruginosa, respectively. In a murine model of Streptococcus pneumoniae type 3 pneumonia, the three Ig preparations were similarly protective. IgGMA was significantly more protective (p less than or equal to 0.025) than Psomaglobin N and Polyglobin N against Salmonella typhimurium in murine peritonitis. However, the mean protective dose (PD50) of the two later preparations was less than or equal to 20 mg/kg body weight. In models of peritonitis both Psomaglobin N and Polyglobin N were more protective than IgGMA (p less than or equal to 0.004) against Haemophilus influenzae b, Klebsiella pneumoniae, Serratia marcescens 06:H3 and group B Streptococcus types 1b and 1c. Psomaglobin N and ciprofloxacin were employed to treat established polymicrobial murine burn wound sepsis resulting from contamination of the burn site with mixtures of P. aeruginosa and Staphylococcus aureus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of gram-negative and gram-positive infections with 3 intravenous immunoglobulin preparations and therapy of experimental polymicrobial burn infection with intravenous Pseudomonas immunoglobulin G and ciprofloxacin in an animal model]. 311 21

A clinical isolate of Pseudomonas cepacia from a cystic fibrosis patient was examined for its ability to produce extracellular toxic material. The organism was grown to stationary phase in a defined medium and toxic material was isolated by ultrafiltration, ion-exchange chromatography on DEAE-Sephacel and gel-filtration chromatography on Sepharose 4B. It consisted of a surface carbohydrate antigen, lipopolysaccharide and protein, and had an LD50 (when injected intraperitoneally into mice) of 395 +/- 20 micrograms. The toxicity appeared to be associated with the lipopolysaccharide portion of the complex, because boiling for 15 min and exposure to proteolytic enzymes had no effect on toxicity. However, saponification destroyed the toxicity of the compound. Studies employing radial immunodiffusion with the sera of mice infected with this organism demonstrated production of the complex in vivo at levels approaching those sufficient to produce death. When sublethal amounts of this complex were placed in the lungs of specific-pathogen-free rats, the lung pathology observed after 12, 24, 36 and 48 h was extensive. However, antibody generated in rabbits against this material could protect mice against the complex, as well as against challenge by the homologous organism. These data indicate that extracellular toxic material produced by P. cepacia may be responsible for the lethality and lung tissue destruction normally associated with an active pneumonia caused by this organism.
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PMID:The importance of extracellular antigens in Pseudomonas cepacia infections. 313 8

The purpose of this investigation was to determine the relative roles of the humoral and cell-mediated immune responses in the resolution of chlamydial genital infection of mice and resistance to reinfection. To this end, female BALB/c mice were rendered B cell deficient by treatment with heterologous anti-immunoglobulin M (IgM) serum from birth. Controls were similarly treated with either normal serum or phosphate-buffered saline. Before inclusion in each experiment, anti-IgM-treated mice were screened for the absence of IgM in serum and for the presence of cell-mediated immune responses. In addition, spleen cells from anti-IgM-treated mice responded to concanavalin A and phytohemagglutinin but not to lipopolysaccharide. By these criteria, mice were designated B cell deficient. B-cell-deficient mice and controls were inoculated intravaginally with a suspension of mouse pneumonitis agent (MoPn), a Chlamydia trachomatis biovar. All B-cell-deficient mice resolved the infection. Additionally, no significant difference was seen in the course of the infection in B-cell-deficient mice when compared with controls. In contrast to control mice, B-cell-deficient mice displayed no detectable antibody responses to MoPn in serum or in genital secretions. However, both B-cell-deficient mice and controls developed delayed-type hypersensitivity and T-cell proliferative responses to MoPn. When challenged 53 days after primary infection, no significant difference was seen in the resistance of B-cell-deficient mice to reinfection when compared with that of the controls. These data indicate that cell-mediated immune mechanisms play an important role in the resolution of and resistance to chlamydial genital infection in this model.
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PMID:Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection. 325 86

The ability of concentrated antibody against the 78- or 40-kilodalton (kDa) outer membrane protein (OMP) of Haemophilus somnus to passively protect calves against H. somnus-induced pneumonia was determined. The 78- and 40-kDa OMPs were evaluated in passive protection experiments, because results of previous studies demonstrated their (i) immunogenicity for cattle, (ii) intense reactivity with convalescent-phase sera which passively protected calves against experimental H. somnus pneumonia, (iii) surface location and accessibility to antibody, and (iv) conservation among a wide range of H. somnus isolates obtained from animals with different diseases and from different geographic locations. The specificity of the two antisera evaluated in this study was verified by (i) immunoblots in which reactivity against the 78- or 40-kDa OMP was present in postimmunization but not preimmunization serum and (ii) immunoblots in which affinity-purified, surface-reactive antibodies in each antisera were used, which demonstrated that essentially only antibody to the 78- or 40-kDa OMP was reactive with the surface of H. somnus. In enzyme-linked immunosorbent assays, the antiserum against the 40-kDa OMP contained immunoglobulin G1 (IgG1), IgG2, and IgM against H. somnus, while the antiserum against the 78-kDa OMP contained IgG1 and IgM but no IgG2 against H. somnus. The antiserum against the 40-kDa OMP contained IgG1 and IgG2 specific for the 40-kDa OMP, as determined by Western blot analysis. Slight reactivity against H. somnus lipopolysaccharide was detected by enzyme-linked immunosorbent assay but not by Western blot analysis. In passive protection experiments, preincubation of bacteria with antibody against the 40-kDa OMP protected calves (P less than 0.025) against H. somnus pneumonia, while antibody against the 78-kDa OMP failed to protect calves against H. somnus pneumonia. Determination of the potential protective capacity of the 78-kDa OMP awaits resolution of the role of anti-78-kDa IgG2 in protection against H. somnus pneumonia. The 40-kDa OMP is, however, a good candidate antigen for evaluation of protective ability against H. somnus pneumonia following active immunization.
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PMID:Protective ability of antibodies against 78- and 40-kilodalton outer membrane antigens of Haemophilus somnus. 341 May 39


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