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Biomedical subjects

I D Gardner

Publications and source records attributed to I D Gardner.

At least 37 records · Page 2Linked to original sources
PubMed1982

Depressed human monocyte function after influenza infection in vitro.

Human monocytes were separated from peripheral blood of 22 normal healthy adults and incubated with Hsw1N1 influenza virus or diluted allantoic fluid. The treated monocyte populations were tested for five parameters of monocyte function. Influenza infection markedly inhibited the monocyte chemotactic response and the killing of Candida albicans; infection also depressed phagocytosis, slightly reduced spreading, but did not affect adhesion to glass. These results suggest that influenza virus may also have an inhibitory effect on monocyte function in vivo and help to explain the increased susceptibility to secondary bacterial infection and the general immunosuppression seen in influenza infection.

Adult↗
PubMed1981

Monocyte function in ageing humans.

Peripheral blood monocytes from hospitalised patients greater than 60 years of age and less than 35 years, and those from healthy normal controls less than 35 years, were tested for a range of functional and physiological properties, comprising chemotaxis under agarose, the ability to phagocytose and kill Candida albicans, adhesion to glass and spreading on glass. No significant difference was found between young and old groups, nor between hospitalized and non-hospitalized groups in respect of any parameter. There was some decline in phagocytosis and in spreading in a very old subgroup (greater than 75 years), but this was not statistically significant. This study showed that phagocytic cell function in the elderly does not decline at the same rate as the specific immune response and thus cannot directly account for the increased incidence of infection in the aged.

Adhesiveness↗
PubMed1981

Suppression of antibacterial immunity by infection with influenza virus.

The effect of influenza virus infection on systemic antibacterial resistance was assessed in a mouse model. Prior infection with influenza virus by the intranasal route led to a reduced level of macrophage activation in response to intravenous challenge with Listeria monocytogenes. Specific immunity to Listeria was measured using adoptive transfer of immune spleen cells. Preinfection of recipient mice with influenza virus reduced the level of adoptive immunity. Influenza virus preinfection of immune cell donors produced a similar decrease, which suggested that specific thymus-derived cell-mediated immunity was impaired in addition to macrophage function. The exact mechanism affected by influenza virus infection was not clear, but there was thought to be a direct effect on the macrophage with a secondary effect on the thymus-derived cell via its accessory role in the specific immune response. The immune parameters studied were still depressed at a time when actual resistance was enhanced, a result which implied that nonimmunologic factors may be involved in the enhanced susceptibility to secondary infection.

Animals↗
PubMed1981

Monocyte function in normal adults. Simplified methods of separation and testing.

Human blood monocytes were separated by centrifugation over modified Ficoll-Hypaque and by this one-step procedure relatively high proportions (mean 54%) and yields of monocytes were obtained. Yields ranged from 0.22 x 10(9) to 0.98 x 10(9/l of blood and averaged 2 1/2 times the theoretical maximum yield calculated from the blood leucocyte and differential counts. A range of tests of monocyte function are described, namely, adhesion to glass, spreading on glass, chemotaxis under agarose and phagocytosis and killing of Candida albicans. These tests are generally simpler to perform than similar tests previously described and give very reproducible results which compare well with those reported by others. Normal values from 35 healthy Chinese adults are recorded.

Adult↗
PubMed1980

Effect of influenza virus infection on susceptibility to bacteria in mice.

A model of combined infection was established with intranasal influenza virus and systemic Listeria monocytogenes infections of mice. Prior infection of mice with influenza virus markedly influenced resistance to subsequent challenge with L. monocytogenes. If mice were infected with influenza virus within the 24-hr period before challenge, a substantial increase in mortality was reflected by enhanced growth of Listeria in the spleen. If mice were infected with influenza virus three or five days before challenge, mortality was decreased, with an accompanying reduction in the growth of Listeria in the spleen. Thus, pulmonary infection with influenza virus has a major effect on susceptibility to systemic infection, exerting a depressive effect on host resistance in the first 48 hr and then causing a longer period of enhanced resistance.

Animals↗
PubMed1980

Histopathological changes in the lungs of influenza-infected mice superinfected with Staphylococcus aureus.

Histopathological changes in the lung were assessed in a model infection of mice using swine influenza virus and Staphylococcus aureus. Virus preinfection markedly enhanced both the persistence of S. aureus and the extent and duration of the inflammatory response. Lymphocytic infiltration was increased and regeneration and squamous metaplasia were delayed, suggesting an enhancement of an immunopathological response to the virus. Mice with the dual infection showed a decrease in phagocytic cell infiltration of the lung compared to that observed in those with the bacterial infection only, and this may reflect a decline in alveolar macrophage function after influenza infection.

Animals↗
PubMed1979

One-way mixed lymphocyte culture: differences between Chinese and Caucasian stimulator cells.

In "standardized" one-way mixed lymphocyte cultures, a pool of blood lymphocytes from randomly chosen Chinese subjects was a significantly stronger stimulus to Caucasian responder lymphocytes than was a pool of allogeneic cells from Caucasians. In contrast, Chinese lymphocytes did not respond more strongly to Caucasian cells than to Chinese cells. This could not be explained by an inherent racial difference in the capacity of blood lymphocytes to undergo blastogenesis. The implications of these findings for organ transplantation and routine testing of cell-mediated immune function are discussed.

Adult↗
PubMed1978

Failure of immunogenic tumors to elicit cytolytic T cells in syngeneic hosts.

Immunogenic, methylcholanthrene-induced sarcomas failed to elicit the production of rapidly cytolytic T lymphocytes in syngeneic mice, although they did elicit the production of more slowly cytotoxic cells. They were, however, susceptible to attack by cytolytic T cells from allo-immune mice and, if infected with ectromelia virus, to attack by similar cells from virus-immune, H-2 compatible mice. It is suggested that the failure to elicit cytolytic T cell production may be due to the lack of an appropriate association between tumour-specific antigens and elements of the major histocompatibility complex.

Animals↗
PubMed1978

Aging and the immune response. I. Antibody formation and chronic infection in Toxoplasma gondii-infected mice.

Studies were performed to determine the effect of aging on the antibody response and cyst formations after infection with a relatively avirulent strain of the intracellular parasite Toxoplasma gondii. When compared with young mice (4 months), aged mice showed a significant decrease in the magnitude of humoral immune response to infection. This decrease was observed at the peak of the acute infection and also during chronic infection. Evaluation of the presence of Toxoplasma cysts, a measure of the latent infection, revealed that the numbers of tissue cysts present 11 weeks after infection increased with the age of the mice at time of infection. The larger numbers of cysts in older mice which had received the same inoculum size of T. gondii as young mice, together with our previous observations of increased susceptibility of these older mice to T. gondii, suggest that an age-related decrease in the early immune response to this infection allows an increased multiplication of the organism in vivo, leading to increased cyst numbers or death.

Acute Disease↗
PubMed1977

Age-related decline in the resistance of mice to infection with intracellular pathogens.

Resistance to infection with Toxoplasma gondii and Listeria monocytogenes in BALB/c female mice decreased with increasing age. The decrease was apparent as early as 9 months of age and was more marked as the animals aged further. This age-related decline in resistance was not restricted to BALB/c female mice, as male and female mice of the C57BL/6 strain exhibited similar responses. With both pathogens, aged mice showed a more marked susceptibility to the strain of lesser virulence. Transfer of normal serum from old mice to young or old mice before infection with T. gondii resulted in an increased susceptibility to this organism, suggesting the presence of inhibitory factors or the absence of potentiating factors that are present in the serum of young mice.

Aging↗
PubMed1976

Cytotoxic T cells in the peritoneal cavity of mice infected with ectromelia virus.

Peritoneal exudate cells from mice infected with ectromelia virus were cytotoxic for virus-infected target cells as measured in a 51Cr release assay. Cytotoxic activity seemed to be T cell-dependent as it was largely abolished by treatment with anti-theta serum and complement but was not impaired by macrophage depletion. The kinetics of development of cytotoxicity in the peritoneal cavity lagged behind spleen cytotoxicity by 1-2 days. Peak activity in peritoneal cells was present about 6 days after intravenous infection with virus. These studies suggest that macrophages present in the free peritoneal cell populations of ectromelia-infected mice are not cytotoxic for virus-infected target cells. The effect of macrophages in virus clearance is therefore likely to be due to phagocytic rather than cytotoxic effects.

Animals↗
PubMed1975

Cell-medicated cytotoxicity against ectromelia virus-infected target cells. III. Role of the H-2 gene complex.

The role of the H-2 gene complex in expression of cytotoxicity exerted by specific ectromelia-immune thymus-derived (T) cells against ectromelia-infected target cells was examined. A repertoire of inbred mouse strains (some congenic) including the H-2 haplotypes k, d, b, s, q, the recombinant H-2a(k/d) and F1 hybrids (k/b and d/b) were immunized with virus and their spleen cells tested 6 days later, at the peak of the primary response, against H-2k,H-2d and H-2b target cells. Significant specific cytotoxicity occurred only when the immune cell donors and the target cells shared all or part of the same H-2 gene complex. For example, H-2a (k/d) immune cells killed both H-2k and H-2d target cells. There was no detectable effect of the non-H-2 genetic background, H-2 public specificities, or the M-locus. Target cells infected with ectromelia virus exhibited quantitative or qualitative changes (or both) in expression of normal H-2 antigens as indicated by reduced susceptibility to killing by T cells activated against H-2 antigens in mixed lymphocyte culture. These data are consistent with the hypothesis that T cells in this system are responding to virus-induced, specific changes in antigens on infected cells which are controlled by genes in the H-2 complex; these genes seem likely to be those coding for H-2 private specificities, or genes closely linked to them.

Animals↗
PubMed1975

Effects of thymus-independent (B) cells and the H-2 gene complex on antiviral function of immune thymus-derived (T) cells.

Antiviral activity in vivo exerted by ectromelia virus-immune spleen cells transferred to ectromelia-infected recipients and cytotoxicity against virus-infected target cells in vitro were both properties of non-immunoglobulin (Ig)-bearing cells (which included T cells). Ig-bearing cells, including thymus-independent (B) cells and antibody-secreting cells, were much less active in vivo when injected alone and tended to block rather than amplify the effect triggered by T cells. Ig-bearing cells were also slightly active in vitro, possibly because some T cells have detectable Ig. Antiviral effects in cell transfer experiments were seen only when immune cell donors and infected recipients shared the same H-2 gene complex. These results are consistent with the hypothesis that the T cell response to ectromelia infection is directed against specific virus-induced change(s) in antigen(s), specified by gene(s) in the H-2 complex, which appear in virus-infected cells.

Animals↗