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Biomedical subjects

K C Bergmann

Publications and source records attributed to K C Bergmann.

At least 55 records · Page 3Linked to original sources

A placebo-controlled, blind comparison of nedocromil sodium and beclomethasone dipropionate in bronchial asthma.

A multi-centre, randomized, blind comparative group study was carried out in 202 adult patients, who had suffered from asthma for at least 2 years, to assess the effectiveness and tolerability of maintenance treatment with either 4 mg nedocromil sodium 4-times daily, 0.1 mg beclomethasone dipropionate 4-times daily or 2 puffs of placebo 4-times daily, given by inhalation. Lung function (FEV1 and sRaw) measurements were made at the beginning and end of a 2-week baseline period and then after 3 and 6 weeks of treatment: assessment were also made of asthma severity. Patients recorded daily on diary cards details of morning and evening PEFR, usage of inhaled bronchodilators, severity of dyspnoea, cough and morning tightness. The results showed that, compared with placebo, both nedocromil sodium and beclomethasone dipropionate-treated patients showed an improvement in FEV1 and a reduction in sRaw values: PEFR increased slightly in all three groups. There was an improvement in asthma severity, diminished rate of dyspnoea and cough, and reduced usage of inhaled bronchodilators in patients receiving active treatment but not in those on placebo. Overall assessment of treatment efficacy by both investigators and patients showed that opinions were significantly in favour of active treatment over placebo. Treatment was well tolerated and no serious side-effects were reported. It was concluded that at the dosages used nedocromil sodium was comparable with and equivalent to inhaled beclomethasone dipropionate in nearly all of the parameters assessed, and both drugs were superior to placebo in the maintenance treatment of asthma in adult patients.

Adolescent↗

[The synergism of Actinobacillus pleuropneumoniae and influenza A virus in experimentally-infected mice].

Models for infecting mice with Influenza A-Virus (A/PR 8/34, H0N1) and Actinobacillus pleuropneumoniae (serotype 9) were developed in Han: NMRI-mice. After infecting mice with sublethal doses of one of the infectious agents, or both together as a mixed infection, animals were subsequently exsanguinated and the lungs washed by bronchoalveolar lavage. Clinical symptoms were recorded daily, examination of lung lavage fluid and sera as well as histology of the lungs were done. An increase in mortality, weight reduction and total cell yield of lung lavage fluid was observed after mixed infection. Compared to mixed infections total protein content and elastase in sera and lung lavage fluid after singular ones were raised not as much. In lung lavage fluid the total cell yield was increased more marked. These alterations indicate a synergistic effect of viruses and bacteria, developed by mixed infection as well as a bacterial infection on top of a viral one. Histopathologically the lung alterations were found to depend on the infectious agent and the mode of infection.

Actinobacillus↗

Enhanced murine respiratory tract IgA antibody response to oral influenza vaccine when combined with a lipoidal amine (avridine).

The adjuvant activity of avridine, a synthetic lipoidal amine, incorporated in liposomes, was studied in mice immunized orally with killed influenza virus vaccine (A/PR/8/34, H1N1). Coadministration of avridine-containing liposomes and viral antigen enhanced the remote-site IgA antibody response in the respiratory tract without a concomitant serum antibody response or side effects. The results support the possible use of mucosal adjuvants for oral immunization against respiratory pathogens.

Adjuvants, Immunologic↗

Age-dependent antibody response in mice and humans following oral influenza immunization.

In order to compare the antibody response in serum and secretions from healthy young subjects and the elderly (greater than 60 years), volunteers were immunized with the commercial inactivated influenza virus vaccine, by the usual (parenteral) route or orally. Also, young and old mice (mean age, 20 months) were orally immunized with live influenza virus. The older mice responded with a very slight rise in their serum and respiratory tract antibody levels compared with the young mice but showed no diminution in protection against lethal viral challenge. Elderly volunteers showed only slight serum antibody responses after parenteral immunization compared with the young. Neither group demonstrated a rise in serum antibody following oral immunization. With respect to the secretory IgA (SIgA) antibody response, certain differences were noted between the young and the elderly: the preimmunization levels of antibody to influenza virus were significantly greater in nasal secretions and saliva in the elderly as compared to the young volunteers, and the salivary antibody response was diminished in the elderly. This lack of a salivary antibody response in the elderly was explicable by the inverse relationship between the preimmunization SIgA antibody titers and the response to immunization. Oral immunization led to no more side effects than observed in the placebo control group.

Administration, Oral↗

Respiratory failure following anti-lung serum: study on mechanisms associated with surfactant system damage.

Within 2 minutes intravenous anti-lung serum (ALS) into guinea pig induces a respiratory failure that is fatal within 30 min. The relationship between surfactant, alveolar-capillary permeability and respiratory failure was studied. Within two minutes ALS induced a leak in the alveolar-capillary barrier. Within 30 minutes 28.3% (controls, given normal rabbit serum: 0.7%) of iv 131I-albumin, and 0.5% (controls 0.02%) of iv surfactant phospholipid tracer were recovered in bronchoalveolar lavage. Furthermore, 57% (controls 32%) of the endotracheally administered surfactant phospholipid became associated with lung tissue and only less than 0.5% left the lung. The distribution of proteins and phospholipids between the in vivo small volume bronchoalveolar lavages and the ex vivo bronchoalveolar lavages were dissimilar: 84% (controls 20%) of intravenously injected, lavageable 131I-albumin and 23% (controls 18%) of total lavageable phospholipid were recovered in the in vivo small volume bronchoalveolar lavages. ALS also decreased lavageable surfactant phospholipid by 41%. After ALS the minimum surface tension increased. The supernatant of the lavage increased the minimum surface tension of normal surfactant. In addition, the sediment fraction of the lavage had slow surface adsorption, and a marked reduction in 35,000 and 10,000 MW peptides. Exogenous surfactant ameliorated the ALS-induced respiratory failure. We propose that inhibition, altered intrapulmonary distribution, and dissociation of protein and phospholipid components of surfactant are important in early pathogenesis of acute respiratory failure.

Animals↗

[Detection of specific antibodies to influenza viruses of the genital tract of mice following oral immunization].

Balb c-mice were immunized orally twice within 10 days with a live influenza vaccine (A PR 8/34, H1 N1). Specific antibodies were determined in sera, uterus homogenates and uterus lavage fluids. In all compartments specific antibodies of IgG class were estimated by means of an enzymimmunoassay. Regarding estrogen cyclus of mice the antibody titers were divided into diestrus, proestrus, estrus and metestrus. We have not seen any cyclic changes of antibody titers. The results support the concept of a common immune mucosal system. The continuous antibody titers during genital cyclus are evident for using oral vaccination aiming to induce secretory antibodies in genital tract.

Administration, Oral↗

Remote-site stimulation of influenza antibodies in monkeys following intestinal stimulation.

Antibodies in nasal secretions and saliva were stimulated in 10 monkeys (Macacus rhesus) which had been immunized orally with a killed influenza vaccine. Prior to immunization, monkeys had no detectable antibody to influenza virus hemagglutinin or neuraminidase in sera or secretions. Oral immunization (6 times within 12 days, total of 0.6 mg hemagglutinin (HA) and 240 neuraminidase units) using intraesophageal intubation induced secretory antibodies to both antigens, but no serum antibody. Six and 8 monkeys reacted with HA-antibodies in nasal secretions and saliva, respectively, whereas neuraminidase antibodies occurred in nasal secretions of all 10 and in the saliva of 9 animals. The results support the concept of a common mucosal immune system in monkeys.

Administration, Oral↗

Secretory antibody following oral influenza immunization.

Secretory IgA antibody may be important in protection against respiratory viral infections, and the concept of a common mucosal immune system offers the theoretical basis for the convenient stimulation of this antibody. Therefore, the oral route was compared with intramuscular injection in a double-blind, placebo-controlled study in young healthy volunteers. A killed influenza vaccine, given in enteric-coated capsules (total of 98 ug hemagglutinin of A/Bangkok) led to significant salivary and nasal IgA antibody rises in a 4-week period. The preimmunization titers in secretions were inversely correlated with the antibody rise after immunization. The orally administered vaccine was associated with no more side effects than placebo, in contradistinction to reactions following the intramuscular route. The latter route also was without significant effect in regard to a stimulation of secretory antibodies. The observed simultaneous induction of antibodies in saliva and nasal secretions following oral administration of killed vaccine gives further evidence of a common mucosal immune system and its possible clinical use.

Administration, Oral↗

[Occurrence of antibodies against influenza viruses in the female genital tract of mice following oral immunization].

Antibodies of IgA-class against influenza viruses were detected by an enzyme immunoassay (ELISA) in uterus homogenates and uterus lavage fluids of NMRI-mice following immunization. Immunization was performed twice by the oral route within 14 days using a live influenza vaccine (A/PR/8/34, H1N1). Specific antibodies were estimated in homogenates as well as in lavage fluids. The results support the concept of a common immune mucosal system with local antibody secretion after remote-site stimulation in the intestinal tract.

Administration, Oral↗

[Interferon induction in lymphocytes using a bacterial lysate].

A polyvalent bacterial lysate (IRS 19) could be shown to induce interferon (IFN) in peripheral mononuclear leukocytes isolated from human and mouse blood by density gradient centrifugation. Upon stimulation with optimal doses of the inducer, the cells of both species produced 1000 to 2000 IU IFN/ml when cultured for up to 72 hours. In both systems the interferon was released to the culture supernatants in a first wave from one to four hours after addition of the inducer and in a second beyond the 16th hour of incubation increasing up to 72 hours, this time, reaching a 10 fold higher titer.

Animals↗

[Long-term effect of oral immunization against influenza with a live vaccine in mice].

NMRI-mice were immunized orally twice within 19 days with live influenza virus (A/PR/8/34). Immunization led to the occurrence of specific antibodies in the respiratory tract detectable at least for 6 months after booster immunization. Immunized animals are protected against aerogenic infection, demonstrable by normal lung cell yield, lack of virus shedding, and survival of all mice. The used doses was lethal for unimmunized controls.

Administration, Oral↗

[Current concepts of the predisposition and pathogenesis of exogenous allergic alveolitis].

The present conceptions about the pathogenesis of extrinsic allergic alveolitis (EAA) are summarized in a review. The development of EAA depends on both intrinsic (predisposing factors like HLA-groups etc.) and extrinsic components (nature of antigen, intensity and duration of the exposure smoking habits). Cell-mediated immunity plays a decisive role in the recognition of antigen, the induction of the pathogenic immune response (imbalance or dysregulation of T-Helper and T-Suppressor cells), in the realizing of the pathogenic effect in the lung tissue (sensitized lymphocytes, synthesis of lymphokins and interleukins with the consequent liberation of enzymes, tissue injury, granuloma-formation, fibrosis). The production of specific antibodies, the formation of immune complexes, the activation of complement system and as well as immediate irritant-toxic effects by the inhaled agents are also important in the pathogenesis of EAA.

Alveolitis, Extrinsic Allergic↗