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Biomedical subjects

F M Collins

Publications and source records attributed to F M Collins.

159 records · Page 9Linked to original sources
PubMed1969

Effect of specific immune mouse serum on the growth of Salmonella enteritidis in mice preimmunized with living or ethyl alcohol-killed vaccines.

The effect of prior opsonization of virulent Salmonella enteritidis on the growth of this organism in blood, liver, spleen, peritoneal cavity, and inguinal lymph node of specific pathogen-free mice prevaccinated with ethyl alcohol-killed S. enteritidis or living S. gallinarum was determined by daily enumeration. Both the vaccines and the challenge inocula were injected by the intravenous, intraperitoneal, or subcutaneous routes to determine the effect of variations in the vaccinating procedure on the level of immunity induced. The survival percentage observed in mice vaccinated with killed organisms varied extensively, depending on the route of challenge. However, simultaneous organ enumeration studies revealed that vaccination with killed organisms failed to prevent the growth of the challenge organism in vivo. On the other hand, virulent S. enteritidis injected into mice vaccinated with living S: gallinarum failed to multiply and was subsequently eliminated. Immunity in these animals was so effective that a subcutaneously injected challenge did not spread beyond the regional node. Immunization with killed organisms slowed but was unable to prevent the spread of such a challenge beyond the draining node involved in the primary immune response. Neither the route of challenge nor the regimen used in the vaccination had any appreciable influence on the level of antibacterial immunity detected in the organs of the reticuloendothelial system at the time of challenge.

Animals↗
PubMed1968

Cross-protection against Salmonella enteritidis infection in mice.

Mice were vaccinated with six strains of Salmonella and two strains of Escherichia coli, as well as with Pseudomonas aeruginosa, Proteus vulgaris, and Serratia marcescens. The amount of in vivo growth of each organism was followed by viable counting techniques on organ homogenates. The vaccinated mice, along with unvaccinated controls, were challenged intravenously with 1,000 ld(50) of a streptomycin-resistant strain of Salmonella enteritidis. The ability of the vaccine to protect the mice against virulent challenge correlated with the ability of the strain to establish a persisting population in the liver and spleen. Enumeration of the liver and spleen populations in the challenged mice revealed that extensive growth of S. enteritidis occurred in animals which showed "protection," as assessed by progressive mortality data. No evidence was obtained for a major role of humoral factors in the cross-protection against intravenous S. enteritidis challenge.

Animals↗
PubMed1968

Recall of immunity in mice vaccinated with Salmonella enteritidis or Salmonella typhimurium.

Mice were immunized with living Salmonella enteritidis or S. typhimurium and then were reinfected 8, 30, 60, and 150 days later with streptomycin-resistant strains of S. enteritidis, S. typhimurium, or a mixture of the two organisms. The level of resistance at the time of challenge and the rate at which resistance was recalled in late convalescence was determined by daily liver and spleen counts of the challenge population. An immediately effective specific antibacterial immunity was maintained only while the vaccinating strain could still be detected in the liver and spleen. Reinfection of vaccine-free mice with the homologous organism caused a rapid recall of antibacterial immunity (within 3 days), but the response to the heterologous organism was much slower (5 to 8 days). Simultaneous injection of both pathogens into the vaccinated mice resulted in liver and spleen growth curves which resembled those obtained when the two organisms were administered separately. The implications of these growth studies in the development of specific cellular immunity to Salmonella infections are discussed.

Animals↗
PubMed1966

Host-parasite relations in mouse typhoid.

The development of acquired resistance to Salmonella typhimurium has been studied in mice infected intravenously with small numbers of streptomycin-sensitive or streptomycin-resistant organisms. By the 14th day of a primary infection the mouse develops a mechanism capable of destroying completely a super infecting dose of organisms, but is unable to eliminate organisms of the primary infection. The latter are constantly returned to the circulation from necrotic foci at the sites of implantation. Passive transfer of serum from actively infected or vaccinated animals, and immunization with heat-killed organisms, increase the capacity of the host to clear organisms from the blood, but do not interfere to any significant extent with their subsequent multiplication in the tissues. It is concluded that the resistance of actively infected animals depends on a nonhumoral mechanism capable of destroying organisms from endogenous or exogenous sources.

Animals↗
PubMed1966

Mechanisms of acquired resistance in mouse typhoid.

Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular S. typhimurium pretreated with immune serum, cells from infected animals killed virtually all ingested organisms and did so at an accelerated rate. Macrophages from Listeria monocytogenes-infected mice were shown to possess similarly enhanced microbicidal activity against S. typhimurium. Furthermore, the growth of S. typhimurium in the liver and spleen was more effectively restricted in Listeria-infected mice than in animals vaccinated with heat-killed S. typhimurium, even though the Listeria-infected animals possessed no demonstrable cross-reacting antibody to S. typhimurium. The lack of resistance in the mice vaccinated with heat-killed organisms could not be attributed to any deficiency of humoral factors, since the serum from these animals was as effective at promoting phagocytosis and killing by macrophages as serum from actively infected (and demonstrably resistant) mice. Conversely, Salmonella-infected mice were totally resistant to intravenous challenge with L. monocytogenes. The level of resistance in individual animals was related to the numbers of residual Salmonellae remaining in the tissues; mice with heavier residual infections being the more resistant. Specific antiserum from mice vaccinated with heat-killed S. typhimurium was found to be significantly protective only when the intraperitoneal route of challenge was employed. The foregoing studies have been interpreted to mean that enhancement of the microbicidal ability of macrophages is the mechanism of major importance in acquired resistance to S. typhimurium infection in mice.

Animals↗
PubMed1966

Infection-immunity in experimental salmonellosis.

Salmonella enteritidis is highly virulent for the mouse causing an infection resembling mouse typhoid. Survivors of the infection are completely resistant to reinfection and eliminate a large challenge dose of virulent organisms within 72 hr. The antigenically related Salmonella gallinarum was almost avirulent for the mouse but animals vaccinated with this organism were equally capable of eliminating a lethal dose of virulent S. enteritidis. Living Salmonella pullorum, on the other hand, was quickly eliminated from the tissues of normal mice. Vaccination with this organism failed to evoke an effective bactericidal mechanism. Alcohol-killed vaccines of these three Salmonellae all produced an increase in blood clearance rate, but gave only marginal protection against S. enteritidis. Liver and spleen counts on these mice revealed a 1 to 2 day delay before any net increase in the total bacterial population could be observed. Immunization of mice with increasing doses of living Salmonella montevideo resulted in progressively greater killing of a challenge dose of S. enteritidis despite the absence of common somatic antigens between the two strains. The degree of protection varied with the size of the residual population of S. montevideo in the vaccinated mice. The significance of these findings in assessing the importance of various factors involved in the development of acquired resistance to Salmonella infections is discussed.

Animals↗
PubMed1966

Heat-labile antigens of Salmonella enteritidis. I. Extraction of antigens.

Milne, Margaret (University of Adelaide, Adelaide, Australia), and F. M. Collins. Heat-labile antigens of Salmonella enteritidis. I. Extraction of antigens. J. Bacteriol. 92:543-548. 1966.-Salmonella enteritidis strains of high and low mouse virulence were grown in continuous culture. Cell walls were obtained from both strains by sonic disruption, and the washed walls were extracted at 4 C with sodium dodecyl sulfate or sodium deoxycholate. The extracts were eluted with a saline gradient from a diethylaminoethyl cellulose column, and the separated peaks were tested for precipitin activity against rabbit antisera prepared with heator ethyl alcohol-killed vaccines. The separated antigens reacted less intensely with the antiserum to heat-killed cells than they did to the antisera prepared against alcohol-killed vaccine. Little antigenic difference could be detected between the extracts prepared from the virulent and the avirulent organisms.

Animals↗
PubMed1966

Heat-labile antigens of Salmonella enteritidis. II. Mouse-protection studies.

Collins, F. M. (University of Adelaide, Adelaide, South Australia), and Margaret Milne. Heat-labile antigens of Salmonella enteritidis. II. Mouse-protection studies. J. Bacteriol. 92:549-557. 1966.-A number of extracts prepared from a virulent and an avirulent strain of Salmonella enteritidis were used to immunize mice. Living and alcohol-killed whole-cell vaccines were also used to compare the relative protective value of the various preparations. All mice were challenged intravenously with 100 to 1,000 ld(50) of S. enteritidis. Daily counts of the liver, spleen, and blood populations of vaccinated and control mice revealed that the challenge organism was rapidly eliminated only in those mice which had been immunized with a living vaccine. Immunization with extracts resulted in rapid clearance of S. enteritidis from the blood, but, after a delay of 24 to 48 hr, the bacterial populations increased until a maximal liver and spleen population of approximately 5 x 10(8) was reached. Between 55 and 100% of the immunized animals died, compared with 95 to 100% of the controls. With all four extracts, it was only the first antigenic fraction eluted from diethylaminoethyl cellulose which had any detectable effect on host resistance. The ineffectiveness of vaccines prepared with the various extracts or with whole killed bacteria relative to the protection observed after immunization with living organisms is discussed.

Animals↗
PubMedDate not supplied

Antituberculous immunity: new solutions to an old problem.

Tuberculosis continues to be a serious public health problem worldwide. In Europe and the United States, it is now primarily a disease of the elderly; the alcoholic; the drug abuser; Central American, African, and Asian immigrants; and patients with AIDS. New and improved antituberculous vaccines are urgently needed, as both prophylactic and therapeutic agents. Recent advances in molecular biology, genetic engineering, and hybridoma technology make it possible to identify and clone the genes thought to be responsible for the production of the protective antigens (or epitopes) of Mycobacterium tuberculosis. These antigens are produced by the pathogen as it multiplies within the lymphoreticular organs of the infected host. The "protective" genes can be transferred to suitable expression vectors by means of shuttle phasmids, making possible the development of specifically tailored vaccines capable of protecting infants and young adults more effectively against pulmonary tuberculosis and immunocompromised individuals against the disseminated form of this disease.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Immune responses to atypical mycobacterial lung infections.

Various species of atypical mycobacteria exhibited a wide range of growth patterns in the lung, liver, and spleen of specific pathogen-free B6D2 mice infected with these organisms. The growth varied from rapid elimination (complete avirulence) to a continued persistence in the lung, which eventually resulted in the death of many of the mice. Prior depletion of the T cells of aerogenically challenged mice did not affect the growth characteristics of the organisms within the lungs. Mice infected with Mycobacterium habana developed an early hypersensitivity response to the cytoplasmic protein antigens (CPA) of this organism, and this response was followed by a persistent state of anergy. Mice infected with Mycobacterium simiae failed to develop detectable levels of hypersensitivity at any time during the study. Spleen cells taken from mice infected with M. habana or M. simiae exhibited an early peak in the incorporation of [3H] thymidine after exposure of the cells to the nonspecific T-cell mitogen phytohemagglutinin (PHA). A similar peak occurred when the cells were exposed to the specific mitogen CPA of M. habana. Later in the infection, the anergic spleen cells showed no transformation of lymphocytes after exposure to either PHA or CPA. T-cell-mixing experiments, which were carried out both before and after treatment of suspensions of cells from the anergic spleens with anti-Thy 1.2 antiserum plus complement, indicated the presence of a population of suppressor T cells in the anergic animals.

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