PubMed Health⌕ Search

Biomedical subjects

J W Osebold

Publications and source records attributed to J W Osebold.

At least 37 records · Page 2Linked to original sources
PubMed1975

Immunochemical analysis of serum-related proteins in the respiratory tract secretions of normal mice.

Normal mouse lung lavage fluid was analyzed for its content of serum-related proteins by the methods of gel filtration, immunoelectrophoresis, and double immunodiffusion. Lavage samples were collected from exsanguinated mice using three repeated infusions of 0.9% sodium chloride solution. Cells were removed, and the lavage fluid was concentrated. Approximately 0.23 mg of protein per mouse was present in the concentrated solution. Albumin, transferrin, and immunoglobulin G (IgG) were among the proteins in greatest concentration. Albumin, IgG1, IgG2, IgA, and IgM were quantitated by single radial diffusion. Although immunoglobulins could be synthesized locally, albumin and transferrin were assumed to come from plasma. The albumin content was used to estimate the amount of transudated plasma as 0.0027 ml per mouse. The IgA levels were low with an IgA/IgG1 ratio of 0.58 and an IgA/IgG2 ratio of 0.43. IgM was not detected. Goat anti-lung lavage serum revealed the presence of additional lung-related proteins.

Animals↗
PubMed1974

Effects of antithymocyte sera and antimacrophage sera on cell-mediated immune reactions in Listeria-infected mice.

The cell-mediated immune responses of allograft rejection, delayed hypersensitivity, and resistance to Listeria monocytogenes were suppressed by injections of antithymocyte serum (ATS), but the immune responses were not significantly altered by antimacrophage serum (AMS) or normal rabbit serum (NRS). Antisera were prepared in rabbits against purified mouse thymocytes and purified peritoneal macrophages. When mice were injected with ATS near the time of skin grafting, allografts survived significantly longer. Similar administration of AMS or NRS failed to alter the course of graft rejection. Decreased footpad swelling indicated the suppression of delayed hypersensitivity in mice injected with ATS 6 days after a sublethal inoculation of Listeria cells. None of the serum treatments affected the ultimate survival of mice infected with a small number of bacteria. Either ATS or NRS was injected into immunized mice 1 day before and 2 days after a challenge inoculation of Listeria cells. Pronounced suppression of delayed hypersensitivity was found in the ATS-treated groups, along with extensive mortalities that reached 100% in the group receiving the largest dose of ATS. All control animals survived and demonstrated strong delayed hypersensitivity reactions. Antimacrophage serum had no significant effect on the three mechanisms of cell-mediated immunity that were tested. The lymphoid cells which mediate delayed hypersensitivity, antimicrobial cellular immunity, and allograft rejection possess antigenic determinants in common with thymocytes.

Animals↗
PubMed1974

Relationship of antimicrobial cellular immunity to delayed hypersensitivity in Listeriosis.

The relationship of antimicrobial cellular immunity to delayed hypersensitivity (DH) was studied in mice antigenically stimulated by living Listeria monocytogenes confined to diffusion chambers in peritoneal cavities or by subcutaneous inoculation of sublethal doses of the organism. Mice showed DH reactions when tested 6 days after inoculation, and reactions were positive for at least 90 days in some mice. DH also became established when the mice were stimulated by antigens diffusing from peritoneal chambers containing viable Listeria. Mice were categorized as DH positive or DH negative if they developed more or less than a 5% increase in foot volume 24 h after the injection of Listeria antigen. Some antigenically stimulated mice did not elicit the DH reaction. Consequently, the animals were arranged as immunized groups (DH positive and DH negative) and Listeria chamber implant groups (DH positive and DH negative). When challenged with L. monocytogenes, all four groups were significantly resistant as compared with controls. Thus, the in vivo tests for immunity and DH did not show direct correlation. The results suggested that antimicrobial cellular immunity can occur as a phenomenon independent of DH. Evidence for antimicrobial cellular immunity as the principle mechanism of resistance in murine listeriosis is discussed with consideration for possible heterogeneity of function by thymus-derived lymphocytes.

Animals↗
PubMed1973

Effects of antithymocyte and antimacrophage sera on the survival of mice infected with Listeria monocytogenes.

Antisera prepared in rabbits against purified mouse thymocytes (antithymocyte serum; ATS) and peritoneal macrophages (antimacrophage serum; AMS) were injected intraperitoneally into Balb/c mice infected with the bacterium Listeria monocytogenes. When administered near the initiation of infection, the ATS significantly decreased the survival time of the animals and increased the mortality rate. When ATS was administered 6 days after a sublethal dose of L. monocytogenes had been inoculated, an overt disease did not evolve. ATS that significantly potentiated primary listeriosis also had high cytotoxicity titers for thymocytes and lymphoid cells from the peritoneal cavity. Although cytotoxic activity against peritoneal macrophages could be demonstrated in lower dilutions of the ATS, this activity did not appear to correlate with the effects of the sera on listeriosis. The injection of AMS did not enhance the infectious process. In some trials more deaths occurred among mice receiving normal rabbit serum than those receiving AMS. All of the AMS had cytotoxic titers against peritoneal macrophages, and the sera were usually inactive against thymocytes and peritoneal lymphoid cells. Listeria was isolated from fatally infected mice with nearly equal success in all of the serum-treated groups, and the serum treatments did not appear to alter the pattern of gross lesions. The afferent limb of the immune response was markedly affected by the presence of antibodies to lymphocytes. However, antibodies reacting with macrophages did not demonstrably enhance the Listeria process, which depends upon cellular immunity as the principal means of acquired host defense.

Animals↗
PubMed1972

Activity of macrophage and neutrophil cellular fractions from normal and immune sheep against Listeria monocytogenes.

Cellular immunity to Listeria monocytogenes infection was studied by assaying for antibacterial activity in fractions of leukocytes collected from the peritoneal cavity, lungs, and mammary glands of immunized sheep. The cells were collected in populations that were largely either macrophages or neutrophils. Mechanically disrupted cells were divided into nuclear, lysosomal, and supernatant fluid fractions and then subjected to freezing and thawing. Comparison with similarly treated rabbit cells showed that greater fragility exists in the lysosomes of sheep cells, as indicated by the amount of acid phosphatase activity released. Inhibition of bacterial growth was assayed in a broth medium at pH 4.6. As expected, nuclear and lysosomal fractions from neutrophils were inhibitory. Some antibacterial activity was found in nuclear fractions of macrophages. The lysosomes of macrophages collected from the peritoneal cavity and the mammary gland did not inhibit the growth of L. monocytogenes. Peritoneal macrophages were allowed to interact with sensitized lymphocytes and an avirulent strain of L. monocytogenes for 4 hr prior to disruption and fractionation, but antibacterial activity was not detected. Pulmonary alveolar macrophages from 5 out of 16 sheep contained Listeria inhibitory activity in their lysosomes. The mechanism was inhibitory but not bactericidal.

Acid Phosphatase↗
PubMed1970

Cellular Responses of Mice to Diffusion Chambers I. Reactions to Intraperitoneal Diffusion Chambers Containing Listeria monocytogenes and to Bacteria-Free Chambers.

Diffusion chambers made with membranes having a pore size of 0.22 mum were implanted in the peritoneal cavities of mice. Chambers that contained no cells induced splenic lymphoreticular hyperplasia and a proliferation of fibroblasts around the chambers. When the chambers contained the bacterium, Listeria monocytogenes, there was strong and continuous chemotaxis of phagocytic cells to the membrane surface. The tendency to incite fibrosis around the chambers containing bacteria produced a tissue reaction resembling a chronic abscess or granuloma. The important difference from a natural lesion was the prevention of direct parasite-host cell interactions. In studies on the pathogenesis of long persisting host-parasite relationships, one might successfully use diffusion chambers to investigate the role of humoral antimicrobial substances as well as the effects of chronic inflammation, with its local concentration of metabolic products and constituents of phagocytic cells. On the other hand, the presence of diffusion chambers in the tissues is an abnormal situation and changes arising from their presence may complicate the interpretations of some experiments.

Journal Article↗
PubMed1968

Cellular immunity of mice infected with Listeria monocytogenes in diffusion chambers.

The importance of bringing live bacteria into intimate contact with macrophages as a prerequisite for establishing cellular immunity was investigated. The bacterium Listeria monocytogenes was shown to replicate and survive in diffusion chambers implanted in the peritoneal cavities of mice. Humoral substances accruing from host responses to diffusing soluble antigens of the microorganism were unable to inactivate the bacteria. The resistance of mice immunized by subcutaneous inoculation of the live organism always exceeded the resistance of mice with Listeria diffusion chamber implants. Animals with sham diffusion chambers were more resistant to a challenge by L. monocytogenes than were normal mice. Host resistance was not significantly different between Listeria diffusion chamber implant groups and sham diffusion chamber implant groups. The results suggested that direct involvement of macrophages with the parasite is necessary to achieve cellular immunity.

Agglutination Tests↗
PubMedDate not supplied

Immunological alterations in the lungs of mice following ozone exposure: changes in immunoglobulin levels and antibody-containing cells.

Ozone was added to the air of the environmental chambers containing specific pathogen-free mice. At levels of 0.5 and 0.8 ppm the oxidant was seen to have inflammatory effects, as shown by rising serum albumin levels in lung lavage fluid. Fluorescein conjugated anti-heavy chain sera were used to detect cells containing IgM, IgG, and IgA in measured lung areas termed Pulmonary Units. Antigenic stimuli occurred along the airways, with significant increases of IgA-containing cells in the bronchus-associated lymphoid tissue. The numbers of IgM- and IgG-containing cells did not increase. Immunodiffusion analyses for immunoglobulins in lung lavage fluid indicated increases of IgG1, IgG2, and IgA in lung secretions. The calculation of changing Ig/Alb ratios suggested that the IgA present was largely the result of local synthesis, while IgG molecules were mainly of serum origin. Possible sources of antigenic stimuli to ozone-exposed lungs are discussed.

Albumins↗