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Biomedical subjects

D A Dean

Publications and source records attributed to D A Dean.

At least 91 records · Page 5Linked to original sources
PubMed1981

Relationship between acquired resistance, portal hypertension, and lung granulomas in ten strains of mice infected with Schistosoma mansoni.

Pronounced differences in resistance to reinfection and pathology were observed among various strains of mice infected with Schistosoma mansoni. When comparing strains, the level of resistance induced by a 12-week infection correlated closely with the degree of portal blood pressure elevation and number of lung egg granulomas, but did not correlate with other pathological parameters or with the number of worms or tissue eggs. Among individual mice of the same strain, however, resistance was proportional to the number of worms and tissue eggs. Nmri strain mice infected for more than a year remained highly resistant to reinfection and continued to shunt eggs into the lungs, but showed considerable resolution of portal hypertension, hepatomegaly and splenomegaly. No association was observed among mouse strains between the mortality resulting from a primary infection and the severity of any of the pathological parameters which were measured.

Animals↗
PubMed1978

Immunization of mice with cobalt-60 irradiated Schistosoma mansoni cercariae.

Parameters of immunization of mice with 60Cobalt-irradiated Schistosoma mansoni cercariae are described and related to protection against subsequent challenge infection. Such immunization was found to be dependent on dose of irradiation, number of immunizing cercariae, and number and time course of infections. Low levels of resistance were obtained with low irradiation doses, in contrast to previous studies in mice. In general, resistance increased with increasing irradiation doses, up to approximately 48-56 Kr. Maximal resistance (70-80%) was induced by a single exposure to 250-500 cercariae, irradiated at a dose rate of 2 Kr/minute to a total dose of 56 Kr, administered percutaneously 4-6 wk prior to challenge. Challenge could be delayed for at least 15 wk after immunization without a decrease in resistance. The resistance obtained was not attributable to a delayed migration of challenge worms.

Animals↗
PubMed1978

Effect of immunization on migration of Schistosoma mansoni through lungs.

Schistosoma mansoni schistosomula migrate through the lungs of infected mice; peak recovery occurs 6 days following infection. When cercariae were irradiated at 60Cobalt doses of 24 to 64 Kr, the number of schistosomula recovered from lungs 6 days after infection decreased in a dose-dependent fashion. The pattern of lung migration of schistosomes irradiated at 56 Kr prior to infection was similar to that of nonirradiated schistosomes, but greatly reduced numbers were recovered. When mice were immunized by a single infection with 56 Kr attenuated cercariae 6 wk prior to challenge, the pattern of challenge migration through the lungs was altered. The number of schistosomes recovered increased rapidly between 2 and 6 days post-infection, and showed a plateau between 8 and 10 days with peak recovery occurring 10 days post-infection. This peak recovery was reduced in comparison to that of non-immunized mice, but did not account for all of the reduction observed at the adult worm stage.

Animals↗
PubMed1978

Resistance of mice to secondary infection with Schistosoma mansoni. I. Comparison of bisexual and unisexual initial infections.

Mice receiving a unisexual primary infection with either sex of Schistosoma mansoni did not develop detectable resistance to reinfection. In contrast, mice receiving a bisexual primary infection developed a high degree of resistance. The number of adult worms developing from the challenge infection was reduced, relative to controls, by 72--100% at challenge times of 6 weeks or greater.

Animals↗
PubMed1978

Resistance of mice to secondary infection with Schistosoma mansoni. II. Evidence for a correlation between egg deposition and work elimination.

Mice reinfected with Schistosoma mansoni 6--8 weeks after a primary infection largely or completely eliminated the second infection prior to the 7-week adult worm stage. In contrast, challenge worm counts were not lower than controls at the 6-day lung schistosomulum stage. At reinfection intervals of 12 or more weeks, worm counts were reduced at both stages. The reduction in lung schistosomulum count was proportional to the number of schistosome eggs present in the lungs, with no significant reduction being detected at any challenge time in mice free of lung eggs. Isolated schistosome eggs injected intravenously into the lungs of normal mice induced moderate to high levels of resistance to infection, while eggs injected subcutaneously or imtraperitoneally did not. It is concluded that the deposition of schistosome eggs in sites encountered by migrating schistosomula may be essential for mice to become resistant to reinfection with S. mansoni.

Animals↗
PubMed1977

Improved assay for monocyte chemotaxis using frozen stored responder cells.

Frozen stored human mononuclear cells were compared with non-frozen cells as responder cells in the monocyte chemotaxis assay. Frozen stored cells were found to inhibit lower background migration, resulting in greater experimental-to-control ratios. The use of frozen cells also greatly improved the speed, standardization of conditions and day-to-day reproducibility of the assay procedure. Frozen cells were at least as sensitive as fresh cells for detecting low chemotactic factor concentrations and were superior for detecting differences in concentration.

Blood Preservation↗
PubMed1977

Decreased binding of cytotoxic antibody by developing Schistosoma mansoni. Evidence for a surface change independent of host antigen adsorption and membrane turnover.

Schistosoma mansoni schistosomula maintained in chemically defined culture media became increasingly resistant to the cytotoxic effects of infected guinea pig serum. Two- and 6-day-old schistosomula recovered from mice showed no uptake of IgG antibody from infected guinea pig serum, as revealed by the indirect fluorescent antibody test. Results from this test remained negative when the schistosomula were tested at 0 C, after exposure to drugs which inhibit synthetic and secretory processes, or after being killed by heat or formalin. In contrast, new schistosomula collected within 3 hr after skin penetration bound IgG from infection serum under all test conditions, and showed increased susceptibility to cytotoxicity after exposure to various drugs. It thus appears that soon after skin penetration schistosomula undergo surface changes which prevent binding of antibody from infection serum. These changes can apparently take place in the absence of host antigens, and once they have occurred, do not depend on worm physiological processes for their function.

Adsorption↗
PubMed1977

Immune response of guinea pigs to Schistosoma mansoni. II. In vitro blastogenesis and macrophage migration inhibition factor production in response to cercarial, adult worm and egg antigens.

Guinea pigs infected with Schistosoma mansoni were tested for in vitro lymphocyte response to schistosome antigens and nonspecific mitogens at various times after infection. Production of macrophage migration inhibition factor by peritoneal exudate cells in response to cercarial, adult, and egg antigens reached a peak between 4 and 8 weeks post-infection and diminished rapidly thereafter. In contrast, peak blastogenic responses of blood lymphocytes appeared later than 8 weeks for all antigens and persisted until at least the 24th week. Blastogenic responses to concanavalin A and phytohemagglutinin P were not significantly different in normal and infected animals.

Animals↗
PubMed1975

Immune response of guinea pigs to Schistosoma mansoni. I. In vitro effects of antibody and neutrophils, eosinophils and macrophages on schistosomula.

Schistosomula of Schistosoma mansoni were rapidly killed in vitro by IgG2 antibodies from serum of schistosome-infected guinea pigs and heat-labile factors present in normal serum. Addition of polymorphonuclear neutrophilic leukocytes greatly increased the rate and degree of killing. Eosinophils and macrophages did not increase the level of killing, though they did react with schistosomula already damaged or killed by antiserum. Neutrophils and eosinophils reacted with schistosomula only in the presence of specific antibody, while macrophages nonspecifically attacked dead schistosomula. Serum antibody levels reached a plateau at approximately 6 weeks after a single infection. Attempts to precoat schistosomula with antibody prior to exposure to complement were largely unsuccessful.

Animals↗