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Biomedical subjects

V L Moore

Publications and source records attributed to V L Moore.

At least 73 records · Page 4Linked to original sources
PubMed1978

Humoral and cellular immune responses in Aspergillus fumigatus pulmonary disease.

This study was designed to evaluate immunologic differences between aspergilloma (A) and allergic bronchopulmonary aspergillosis (ABPA), comparing the results to atopic and nonatopic control subjects. Humoral studies included skin tests with common inhalant antigens and Aspergillus fumigatus. Total and specific IgE and other immunologlobulin levels and serum precipitins were evaluated against A. fumigatus. Cellular immunity was studied with routine skin testing and phytohemaqglutinin-induced lymphocyte blast transformation. Antigen-induced blast transformation was also carried out with the use of serial dilutions of A. fumigatus. All patients with ABPA were atopic and had marked elevations of IgE. None of the patients were atopic and they had normal IgE levels. Immediate and late skin reactivity to A. fumigatus was low in control and A groups but high in 2 patients with ABPA. IgG antibody against A. fumigatus was generally greater in the ABPA group. Both ABPA and A had serum precipitating antibody against A. fumigatus. The atopic controls had elevated IgE levels and immediate skin test reactivity to A. fumigatus, and one also had weak serum precipitins against A. fumigatus. IgE antibody against A. fumigatus was generally higher in ABPA than A. ABPA and A patients had elevated stimulation indices (SI) to A. fumigatus. No stimulation could be detected with cells from control subjects. This study indicates that both T and B cell sensitization may play a role in the development of or as a response to aspergillus-related pulmonary disease.

Antibody Formation↗
PubMed1978

Anaphylaxis in isolated rabbit lungs.

Lungs from rabbits sensitized to ovalbumin or bovine gamma-globulin were isolated and perfused with autologous blood. The response to antigen challenge via the perfusate was immunologically specific and characterized by a marked increase in perfusion resistance, a moderate increase in airway resistance and a small decrease in lung compliance. The response could also be elicited by specific antigen challenge in lungs from sensitized rabbits perfused with blood from normal rabbits and in lungs from normal rabbits perfused with blood or plasma from sensitized rabbits. The magnitude of the response was greater when blood or plasma from sensitized animals was used as the perfusate. Therefore, blood and/or plasma factors appear to be the major contributors to the response.

Airway Resistance↗
PubMed1978

Cell-mediated immunity in the lungs of rabbits using conjugated proteins.

A study using direct macrophage migration inhibition of cells from the lower respiratory tract of rabbits immunized with conjugated proteins, incorporated into a killed BCG-oil emulsion, revealed that the reaction was largely carrier specific. The only exception was when bronchoalveolar cells (BAC) from animals immunized with dinitrophenol coupled to ovalbumin (DNP-OA) were significantly immobilized with DNP coupled to bovine gamma-globulin (BGG) in which the ratio of DNP/BGG was high [DNP-BGG(H)]. This result could not be explained by a toxic effect or by a high net negative charge on DNP-BGG(H). In addition, inhibition of BAC from DNP-OA-immunized rabbits was not observed when the ratio of DNP to BGG was reduced approximately 5-fold.

Animals↗
PubMed1978

Absorption of inhaled antigen into the circulation of isolated lungs from normal and immunized rabbits.

The purpose of this study was to determine whether the absorption of inhaled antigen (Ag) across the pulmonary air-blood barrier of the isolated perfused lung can be modulated by immunologic mechanisms. Lungs from immunized or nonimmunized rabbits were removed, ventilated, and perfused with autochthonous blood. Radioiodinated Ag (human serum albumin or ovalbumin) was introduced as an aerosol into the isolated lung for 15 min and blood samples were taken over a 4-h period. The results showed that radioactivity fom inhaled Ag entered the perfusing blood as two fractions. One fraction was precipitable by 5% trichloroacetic acid or antiserum. The TCA-soluble fraction chromatographed differently from iodide and may have represented metabolites of the Ag. Immunization specifically reduced the amount of antigenically intact protein entering the blood. On the other hand, the metabolite reached higher concentrations in the blood of immunized lungs. We conclude that the alveolar capillary barrier of the normal rabbit lung could provide a significant route of entry for inhaled antigen into the systemic circulation and that immunization reduces absorption via this route and enhances pulmonary metabolism of the Ag.

Absorption↗
PubMed1978

Immunologic block against antigen absorption from isolated perfused rabbit lungs.

In previous studies with isolated perfused rabbit lungs, we observed that inhaled human serum albumin (HSA) or ovalbumin (OA) entered the pulmonary circulation antigenically intact. The inhaled proteins were also metabolized in the lung. Immunization reduced the amount of intact protein and increased the amount of metabolites absorbed. In the present study, we have begun to characterize the immune mechanisms responsible for reduced antigen absorption. A humoral immune mechanism appeared to be involved because the phenomenon could be passively transferred to normal animals by administering immune serum either 18 hr or immediately before antigen inhalation. The reduction was also observed when lungs from immunized rabbits were perfused with normal rabbit blood, indicating that antibodies in both lung and blood may be involved. Experiments, in which lungs from immunized rabbits were simultaneously insufflated with the immunizing antigen and with a nonspecific protein, demonstrated that the block against antigen absorption was specific for the immunizing antigen and was not due to some antigen-induced nonspecific changes in lung physiology.

Absorption↗
PubMed1977

Antigens in pigeon breeder's disease: the use of pigeon dropping antigens in detecting antibody activity.

Sera from patients with pigeon breeder's disease were analysed for precipitating antibodies by immunodiffusion and immunoelectrophoresis using whole pigeon dropping extract (PDE) and a purified fraction of PDE (PDE1) as antigens. For comparison, sera from asymptomatic pigeon breeders and normal individuals were also tested for precipitating antibodies. Whereas whole PDE formed precipitin lines with normal serum as well as with serum from symptomatic and asymptomatic pigeon breeders, PDE1 formed precipitin lines only with serum from individuals exposed to pigeons, This suggests that whole PDE forms non-specific (non-antigen-antibody reactions) as well as specific precipitin lines, while PDE1 appears to form only specific lines. These data indicate that whole PDE has limited usefulness in studies of pigeon breeder's disease. It is also possible that PDE1 will be useful in studies of this disease.

Alveolitis, Extrinsic Allergic↗
PubMed1977

Strain variation in BCG-induced chronic pulmonary inflammation in mice. I. Basic model and possible genetic control by non-H-2 genes.

C57BL/6 mice (haplotype H-2b) responded in a dose-dependent fashion to killed BCG by marked enlargement of the spleen and lung. Neither CBA nor C3H mice (haplotype H-2k) responded to such treatment. Pulmonary inflammation in responder B6 animals was characterized by a marked chronic interstitial and alveolar granulomatous process, and was accompanied by occasional granulomata, hyperemia, and loss of architecture in the spleen. Inflammation in non-responder CBA and C3H animals was minimal in both the lung and spleen. The response does not appear to be controlled by genes within the major histocompatibility complex, but is associated with a C57 background. B10.BR mice (responder background, H-2k) were responder animals and C3H.SW mice (nonresponder background, H-2b) were nonresponders. In addition, all animals tested with a C57 background were responders even though two of these strains were not H-2b (C57BL/Ks, H-2d and C57Br/cd, H-2k). The resolution of the mechanism of genetic control of this response in mice may provide information relevant to possible genetic control of chronic pulmonary inflammation in man.

Animals↗
PubMed1976

Immunologically induced lung disease in guinea pigs. A comparison of ovalbumin and pigeon serum as antigens.

This study was conducted to compare the capacity of pigeon serum (PS), an antigen (Ag) associated with hypersensitivity pneumonitis (HP), and ovalbumin (OA) in the induction of immunologic lung disease in guinea pigs (gp). Whereas OA was very effective in inducing a severe pneumonitis, PS failed to produce significant disease. A determination of the antibody (Ab) responses in OA- or PS-sensitized GP revealed that total Ab activity, as well as specific IgG1, and IgG2 responses, were not significantly different in the two groups. There was, however, a markedly higher IgE-like Ab response to OA than to PS. Thus, there was a striking correlation between specific IgE synthesis and the production of immunologic lung disease. The disease resembled immune complex disease histologically, and we suggest that the IgE antibody may function as a preceding "anaphylactic trigger" mechanism for the lodging of complement-fixing Ag-Ab complexes in the vasculature of the lung. It is further suggested that PS may be a poor Ag for the induction of IgE synthesis in guinea pigs.

Animals↗
PubMed1975

Cell-mediated hypersensitivity in pigeon breeders.

This investigation was carried out to study possible differences in cell-mediated hypersensitivity between symptomatic and asymptomatic pigeon breeders. A variety of pigeon antigens were investigated using the indirect migration inhibition test. Cell-mediated hypersensitivity to pigeon antigens was detected in 6 of 8 symptomatic pigeon breeders, and in only 2 of 12 asymptomatic pigeon breeders. The results suggest that cellular mechanisms may be important in the pathogenesis of pigeon breeder's disease.

Animals↗
PubMed1975

An animal model of hypersensitivity pneumonitis in the rabbit.

This study was devised to produce an animal model of hypersensitivity pneumonitis in order to study both the induction and the elicitation of the disease. Rabbits exposed by aerosol to large quantities of pigeon antigens developed a humoral, but not cellular, immunologic response. Moreover, their lungs were essentially normal histologically. A single i.v. injection of killed BCG in oil permitted the induction of pulmonary cell-medid hypersensitivity to the inhaled antigen, as well as the development of pulmonary lesions which were more severe than that caused by the administration of BCG alone. The humoral immunologic response to the inhaled antigen was not increased after BCG injection. Since many individuals are exposed to the etiologic agents of hypersensitivity pneumonitis for extended periods without developing the disease, these findings in animals suggest that some event may occur to induce cell mediated hypersensitivity in order to initiate the disease process. In addition, we have shown that animals with normal lung histology and circulating complement-fixing antibodies undergo serum complement (CH50) depression after an aerosol challenge with the specific antigen. Animals with circulating, complement-fixing antibodies, and inflamed lungs (BCG-induced failed to undergo a complement depression subsequent to an aerosol challenge with specific antigens. These results re consistent with those seen in symptomatic and asymptomatic pigeon breeders and suggest that antigen distribution through the lung is important in the pathogenesis of hypersensitivity pneumonitis.

Acute Disease↗
PubMed1975

Immunoglobulin allotypes in symptomatic and asymptomatic pigeon breeders.

Comparison of immunoglobulin allotypes were studied in a group of patients with pigeon breeder's disease and in similarly exposed by asymptomatic individuals. The study revealed that the disease is not correlated with immunoglobulin allotypes. Furthermore, the phenotype Gm(a;g) was not associated with high levels of serum antibodies to pigeon antigens.

Adolescent↗
PubMed1975

Immunologic studies in hypersensitivity pneumonitis--quantitative precipitins and complement-fixing antibodies in symptomatic and asymptomatic pigeon breeders.

Quantitative precipitation and complement fixation tests were performed on sera from a group of patients with hypersensitivity pneumonitis (pigeon breeders' disease). Their antibody levels were compared to a selected group of similarly exposed but asymptomatic subjects. The quantity of precipitating antibodies was generally greater in serum from symptomatic breeders, although quantities in the serum from some of the asymptomatic subjects were greater than that seen in ill breeders. Complement-fixing antibodies were detected in the serum of both groups. Here again, complement-fixing activity was generally greater in the serum of ill breeders. However, one asymptomatic breeder showed complement-fixing activity greater than most of the symptomatic breeder group. These findings indicate that the presence of complement-fixing antibodies per se in serum to pigeon gamma-globulin is not sufficient to cause the symptoms of pigeon breeders' disease. We suggest that other factor(s) may be involved, such as lgE- or cell-mediated hypersensitivity.

Animals↗