Uptake and transport of horseradish peroxidase by lymphoepithelium of the bronchus-associated lymphoid tissue in normal and bacillus Calmette-Guérin-immunized and challenged rabbits.
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Biomedical subjects
Publications and source records attributed to Q N Myrvik.
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Supernatant fluids from cultures of BCG-sensitized rabbit lymph node and spleen cells contained a factor that strongly agglutinated normal rabbit alveolar macrophages within 3 min at room temperature. In contrast, fluids from nonsensitized cell cultures did not agglutinate normal rabbit alveolar macrophages. This factor was designated macrophage-agglutinating factor (MAgF) because it is similar to the previously described factor found in lung lavages of rabbits exhibiting a BCG-induced pulmonary delayed hypersensitivity reaction. The kinetics of MAgF production in vitro by sensitized lymph node cells and its inhibition by puromycin and actinomycin D suggest active synthesis; sensitized spleen cells exhibited kinetics resembling release rather than synthesis. Studies on purified lymphocyte and macrophage populations from sensitized spleen and lymph nodes indicated that lymphocytes are responsible for MAgF production. However, MAgF production was not induced in normal cells incubated in vitro with concanavalin A or phytohemagglutinin. Fractionation of cell culture supernatant fluids in Sephadex G-100 or Ultrogel AcA-34 clearly separated MAgF from migration inhibition factor; MAgF was present in the void volume of the eluates, suggesting a molecular weight of over 400,000, whereas migration inhibition factor was recovered in the same peak as albumin. The role of MAgF in vivo is unknown, but it is postulated that it may cause the adherence of macrophages during granuloma formation.
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The topography of alveolar macrophages (AM) attached to glass or to Millipore filters was scanning electron microscopy. The cells were obtained from normal and from BCG-vaccinated rabbits. Macrophages that adhered to glass tended to spread while essentially all of the cells that adhered to the Millipore filters remained rounded. The surface morphology of AM attached to Millipore filters closely resembles the morphology of these cells when viewed in situ on the alveolar wall. The use of Millipore filters to study the effect of microbial or host products on cell surface alterations of AM is discussed.
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Fractions of the tubercle bacillus were examined for their capacity to produce an allergic pulmonary granulomatous response in rabbits. We found that emulsions containing old tuberculin and even old tuberculin alone in an emulsion could induce a pulmonary inflammatory reaction comparable in intensity to that produced with killed BCG. Emulsions lacking old tuberculin failed to produce an allergic pulmonary inflammatory response. The significance of these results in relation to immunological and nonimmunological chronic inflammation is discussed.