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)

Mice immunized intransally or intragastrically with proteosome vaccines containing either Shigella sonnei or S. flexneri 2a lipopolysaccharide were protected against lethal pneumonia caused by homologous organisms in an experimental murine intranasal challenge model of Shigella infection. Histopathological analysis demonstrated that immunization also protected against the progressive lesions resulting from invasion of the pulmonary mucosa by S. sonnei. These data show that mucosal proteosome-lipopolysaccharide vaccines can protect against lethal bacterial pneumonia and indicate that such vaccines are promising candidates for protection against intestinal shigellosis.
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PMID:Intransal or intragastric immunization with proteosome-Shigella lipopolysaccharide vaccines protects against lethal pneumonia in a murine model of Shigella infection. 776 27

Endotoxin(lipopolysaccharide = LPS), cell wall component of gram-negative bacteria, activates monocytes and macrophages to release cytokines, reactive nitrogen intermediates (RNI), and to generate tissue factor(TF) which initiate coagulation. We have purified 7kDa and 18kDa cationic antibacterial proteins (CAP-7 and CAP-18) with LPS-binding and LPS-neutralizing activities from rabbit granulocytes using as an assay the agglutination of erythrocytes coated with Re-LPS. From protein sequencing, CAP-7 was identified as the C-terminal 37 amino acid fragment of CAP-18. Synthetic peptide #197 (identical sequence to CAP-7, Gly1-Try37) and #36-1 (a truncation of CAP consisting of 32 amino acid residues, Gly1-Ala32) showed LPS-binding activity. Each peptide inhibited LPS-induced tissue factor(TF) generation by murine peritoneal macrophages, even added 1-3 hours after stimulation of cells with LPS. C57BL/6 mice treated with #197 were significantly protected from lethal LPS challenge. Peptide #36 also blocked the LPS-induced lethality. These peptides had antibacterial activity to gram-negative bacteria, such as E.coli, S.typhimurium, K.pneumonia, Ps.aeruginosa and also to gram-positive S.aureus (Methicillin sensitive and resistant strains). Both peptides inhibited TF- and Xa-induced plasma clotting. Using synthetic chromotogenic substrates, both CAP7 peptides blocked the coagulation cascade at two sites, activation of factor X to Xa and conversion of Factor II (prothrombin) to factor IIa (thrombin). In vivo treatment of peptide #197 prevented acute lethality in mice injected with tissue factor (rabbit brain thromboplastin). Two other peptides, #32(Gly1-Phe9) and #50(Ile13-Typ37) failed to demonstrate LPS-binding, LPS-neutralizing, antibacterial and anticoagulant activities. The active peptides but not the inactive peptide maintain a putative heparin binding domain at their N-termini. This heparin binding domain is participate in the LPS-binding, LPS neutralizing, antibacterial and anticoagulant activities of CAP7. These active peptides may have a therapeutic potential for treatment for DIC due to sepsis and endotoxin shock.
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PMID:Endotoxin-binding synthetic peptides with endotoxin-neutralizing, antibacterial and anticoagulant activities. 783 55

A sandwich ELISA was developed specific for human bactericidal/permeability-increasing protein (BPI), using Mg++ ions to abrogate disturbance by lipopolysaccharide of BPI measurement and to prevent aspecific adherence of BPI to solid phase. In fresh EDTA or heparinized plasma of healthy volunteers BPI was not detectable, whereas in serum BPI was present, indicating that coagulation activates polymorphonuclear leukocytes to release BPI. Furthermore, BPI was present in plasma of critically ill intensive care unit (ICU) patients, in bronchoalveolar lavage fluid of patients suspected of having pneumonia, in wound fluid, and in pleural fluid. In sub-groups of samples with culture-proven bacteria, mean BPI levels were increased compared with subgroups without bacteria, although the differences were only significant in EDTA plasma of ICU patients. These findings indicate the presence of BPI during pathologic conditions. The physiologic role of the released BPI has to be further elucidated.
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PMID:Presence of bactericidal/permeability-increasing protein in disease: detection by ELISA. 787 32

Currently recommended methods in Legionnaires' disease serology are based upon crude whole-cell antigenic preparations. To investigate whether purified antigens would perform better in a given diagnostic test for antibodies against Legionella pneumophila, we compared the performance of three antigenic preparations of L. pneumophila serogroup 1 consisting of outer membrane protein (OMP), flagellin (FLA), and lipopolysaccharide (LPS) to a sonic extract (SON) in indirect immunosorbent assay (ELISA) measuring both IgG, IgA, and IgM. The reactivity of sera from 20 patients with culture-verified Legionnaires' disease and sera from 12 patients with pneumonia and a diagnostic rise in titre by a microagglutination test (MA) was studied. Our results indicated that the SON IgA assay was the most sensitive test in both groups of patients. The LPS IgG and IgM assays, however, were the most specific tests, closely followed by the corresponding SON tests. By combining two individual assays, a maximum nosographic sensitivity of 85% could be obtained. Whereas no benefit of using purified outer membrane protein or flagella instead of a sonic extract in the indirect ELISAs was found, the LPS antigen provided a sensitive and specific alternative to the sonic extract.
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PMID:Performance of four different indirect enzyme-linked immunosorbent assays (ELISAs) to detect specific IgG, IgA, and IgM in Legionnaires' disease. 791 19

To determine the role that the host response to the chlamydial 60 kDa heat shock protein (hsp) plays in the pathogenesis of infertility, C3H/HeN (H-2k) and C57BL/6 (H-2b) mice were inoculated in the left ovarian bursa with 1 x 10(5) inclusion forming units of the Chlamydia trachomatis mouse pneumonitis (MoPn) biovar, and in the right ovarian bursa with mock-infected HeLa-229 cell extracts. Control mice were inoculated with mock-infected HeLa-229 cell extracts. These two strains of mice were chosen because the C3H mice mount a strong immune response to the 60 kDa hsp, whereas the C57BL/6 mice respond only weakly. Vaginal cultures obtained after inoculation were positive for 4 weeks in both strains of mice. Histological sections showed a marked acute inflammatory infiltrate that permeated all the layers of the oviduct and lasted for approximately 2 weeks in both strains. By the third week, mononuclear inflammatory cells were also observed and from 4 weeks after inoculation, hydrosalpinx formation was observed, particularly in the C3H mice. An inclusion immunofluorescence assay detected antibodies specific for chlamydia in the serum and the vaginal washes of the C3H and C57BL/6 mice. Western blot analysis of the serum samples showed an immune response to lipopolysaccharide, and the 30, 40 (major outer membrane protein) and 60 kDa cysteine-rich protein in both strains of mice. In addition, in the C3H mice a strong immune reaction was mounted against a 50 kDa component and the 60 kDa hsp. Six weeks after inoculation, the female mice were mated with male mice of proven fertility and the outcome of the pregnancies evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of infertility by the Chlamydia trachomatis mouse pneumonitis biovar in strains of mice that differ in their response to the 60 kDa heat shock protein. 793 61

Nitric oxide (NO) is produced by murine macrophages in response to cytokines and/or gram-negative bacterial lipopolysaccharide. NO induction by gram-positive bacteria such as group B streptococci (GBS), the major etiologic agents of neonatal pneumonia and meningitis, has received little study. GBS as well as two other gram-positive bacterial species, Staphylococcus aureus and Staphylococcus epidermidis, were found to stimulate NO production in thioglycolate-elicited murine macrophages and in the mouse macrophage cell line J774A.1 in the presence of gamma interferon. Serotype Ia and III GBS were both stimulatory, as were asialo- and type antigen-deficient mutant strains of type III GBS. NO production was dose dependent, inhibitable by L-arginine analogs, and unaffected by polymyxin B. Since phagocytosis by murine and human phagocytes of GBS is dependent on complement receptor type 3 (CR3), the role of CR3 in the NO response to GBS was tested in the CR3-deficient myelomonocytic cell line WEHI-3. GBS did not induce NO, whereas S. aureus or lipopolysaccharide did induce NO in WEHI-3 cells. S. epidermidis, whose nonopsonic phagocytosis is also CR3 dependent, failed to induce NO in WEHI-3 cells. Monoclonal anti-CR3 (anti-CD11b or anti-CD18) in the presence of interferon also induced NO production in thioglycolate-elicited macrophages and in J774A.1 cells but not in WEHI-3 cells. This evidence suggests that ligated CR3 and gamma interferon act synergistically to induce NO production and that CR3 mediates the GBS-induced signal for NO production in interferon-treated macrophages.
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PMID:Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent. 803 77

Female BALB/c mice were immunized intranasally with the mouse pneumonitis biovar of Chlamydia trachomatis and subsequently challenged in the ovarian bursa (C. trachomatis immunized, C. trachomatis challenged). Two groups of mice served as controls. One group was sham immunized intranasally with mock-infected HeLa 229 cell extracts and was challenged in the ovarian bursa with C. trachomatis MoPn (sham immunized, C. trachomatis challenged). The second control group was sham immunized and not challenged (sham immunized, nonchallenged). Before challenge, the C. trachomatis-immunized, C. trachomatis-challenged animals mounted a significant humoral response as shown by high immunoglobulin G (IgG), IgM, and IgA levels and high levels of neutralizing antibodies in serum and moderate IgG and IgA titers in vaginal secretions. Reactivity by Western blot (immunoblot) to the lipopolysaccharide, 30-, 40- (major outer membrane protein), and 60-kDa cysteine-rich proteins and 75- and 100-kDa chlamydial components could be demonstrated. However, reactivity to the 60-kDa heat shock protein was only observed 22 days after challenge. In addition, this group of animals mounted a significant immune response to chlamydial antigens, as shown by a lymphocyte proliferation assay, compared with the sham-immunized nonchallenged mice. After intrabursal challenge, there was no C. trachomatis shedding from the vagina in the C. trachomatis-immunized, C. trachomatis-challenged animals, while 63% of the sham-immunized, C. trachomatis-challenged mice had a positive C. trachomatis culture. In addition, histological sections from the genital tract showed, at 2 weeks postchallenge, a marked acute inflammatory reaction in the sham-immunized, C. trachomatis-challenged animals while in the C. trachomatis-immunized, C. trachomatis-challenged mice there was minimal inflammatory reaction. When the animals were mated, only 12% of the mice from the sham-immunized, C. trachomatis-challenged mice were fertile. In contrast, 94 and 80% of the sham-immunized, nonchallenged and C. trachomatis-immunized, C. trachomatis-challenged mice, respectively, were fertile.
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PMID:Protection against infertility in a BALB/c mouse salpingitis model by intranasal immunization with the mouse pneumonitis biovar of Chlamydia trachomatis. 803 6

The in situ inflammatory response developing in the human lung during a localized bacterial infection was studied in 15 patients with unilateral community-acquired pneumonia (CAP). The local response in the involved lung was compared with that in the contralateral, noninvolved lung as well as with the systemic blood response. Eight healthy volunteers served as control subjects. Concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) were measured by ELISA in bronchoalveolar lavage (BAL) fluids (n = 15), serum (n = 15), and alveolar macrophage and monocyte culture supernatants (n = 8). The concentrations of TNF-alpha, IL-beta and IL-6 in BAL fluid were significantly higher in the involved lung than in the paired noninvolved lung (p < or = 0.01) or in healthy subjects (p < or = 0.02, p < or = 0.01, and p < or = 0.001, respectively). Serum IL-6 concentrations were higher in patients than in control subjects, whereas IL-1 beta and TNF-alpha concentrations did not differ in the two groups. Alveolar macrophages from the involved lung spontaneously released higher concentrations of IL-1 beta, IL-6, and TNF-alpha (p < or = 0.05) than did macrophages from the noninvolved lung, which served as controls. However, macrophages were hyporesponsive in terms of cytokine production to further stimulation by lipopolysaccharide (LPS) in the noninvolved and involved lung compared with controls, whereas peripheral blood monocytes were not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compartmentalized cytokine production within the human lung in unilateral pneumonia. 808 41

The family Pasteurellaceae Pohl contains Gram-negative, facultatively anaerobic and fermentative bacteria of the genera Pasteurella, Haemophilus, and Actinobacillus. Approximately 20 different species of the genus Pasteurella have been identified using phenotypic and genetic analyses. Of these species, P. multocida and P. haemolytica are the most prominent pathogens in domestic animals causing severe diseases and major economic losses in the cattle, swine, sheep, and poultry industries. Mechanisms of immunity to these bacteria have been difficult to determine, and efficacious vaccines have been a challenge to develop and evaluate. Pasteurella multocida of serogroups A and D are mainly responsible for disease in North American poultry and pigs and to a lesser extent in cattle. Fowl cholera in chickens and turkeys is caused by various serotypes of P. multocida serogroup A and characterized by acute septicemia and fibrinous pneumonia or chronic fibrinopurulent inflammation of various tissues. Current biologicals in use are live P. multocida vaccines and bacterins. Potency tests for avian P. multocida biologicals are a bacterial colony count for vaccines and vaccination and challenge of birds for bacterins. Somatic antigens, particularly lipopolysaccharide (LPS), appear to be of major importance in immunity. In North American cattle, P. multocida serogroup A is associated mainly with bronchopneumonia (enzootic pneumonia) in young calves; however, it is occasionally isolated from fibrinous pleuropneumonia of feedlot cattle (shipping fever). Biologicals currently available are modified-live vaccines and bacterins. The potency test for vaccines is bacterial colony counts. The test for bacterin potency is vaccination and challenge of mice. Important immunogens have not been well characterized for P. multocida infection in cattle. In swine, P. multocida infection is sometimes associated with pneumonia; however, its major importance is in atrophic rhinitis. A protein toxin (dermonecrotic toxin), produced by toxigenic strains of P. multocida types A and D, and concurrent infection with Bordetella bronchiseptica appear to be the major factors in development of atrophic rhinitis. Currently available biologicals are bacterins and inactivated toxins (toxoids). The toxin appears to be the major immunogen for preventing atrophic rhinitis. There are, however, no standardized requirements for potency testing of P. multocida type D toxoid. Various serotypes of P. haemolytica biotype A are responsible for severe fibrinous pleuropneumonia of cattle and sheep, occasionally septicemia of lambs, and mastitis in ewes. Several serotypes of P. haemolytica biotype T are isolated from acute septicemia of lambs. The currently available P. haemolytica biologicals are modified-live vaccines, bacterins, bacterial surface extracts, and culture supernates that contain an exotoxin (leukotoxin).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunogens of Pasteurella. 811 91

Tumor necrosis factor-alpha (TNF) is an important humoral mediator of sepsis and endotoxin-induced shock. However, Streptococcus pneumoniae, a gram-positive organism, is the most common causative agent of community-acquired pneumonia and sepsis. We hypothesized that the pathogenesis of pneumococcal pneumonia and sepsis involves pneumococcus-stimulated TNF synthesis, and we tested that hypothesis in vitro by comparing heat-killed type III and type V pneumococcus and 23-valent purified pneumococcal capsular polysaccharides with Escherichia coli and purified lipopolysaccharide (LPS) as stimuli for TNF production by the murine macrophage cell line RAW 264.7. We evaluated TNF production in response to various doses and times of exposure to these agents, as well as the effects of indomethacin on TNF production in response to these agents. Stimulation with both types of heat-killed pneumococcus resulted in TNF production in a dose-response fashion, as did stimulation with E. coli. Fewer type III pneumococci (10 bacteria/ml) were required to stimulate significant TNF secretion than either type V pneumococcus or E. coli, but the overall dose-response curves of the three bacteria were similar. The dose-response curves for pneumococcal capsular polysaccharides and LPS were very similar, although at the highest concentration pneumococcal capsular polysaccharides stimulated more TNF secretion than did LPS (469 versus 213 U/ml). The kinetics of pneumococcus-stimulated TNF secretion were identical to the kinetics of LPS-stimulated TNF secretion. In the presence of indomethacin, pneumococcus-stimulated TNF production decreased by 87.5%, as compared with pneumococcus alone. In contrast, LPS with indomethacin stimulated 19.5% more TNF than LPS alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heat-killed pneumococci and pneumococcal capsular polysaccharides stimulate tumor necrosis factor-alpha production by murine macrophages. 811 47


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