Immunosuppression as a homeostatic mechanism in disease and aging.
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Aging↗
Biomedical subjects
H R Strausser
Publications and source records attributed to H R Strausser.
Altered immune reactivity in encephalomyocarditis-M variant (EMC-M)-induced diabetes in mice.
Approximately 50% of DBA/2j male mice infected with EMC-M develop glycosuria with suppressed immune responsiveness to the mitogens PHA, Con A and PWM. The greatest degree of suppression was noted with Con A treated cultures. In vivo treatment with Levamisole, a known T cell stimulant, especially increased the response to Con A but exacerbated the diabetogenic state as reflected by increased occurrence of glycosuria. Virus infected mice, given anti-lymphocyte serum (ALS), showed marked amelioration of the diabetic syndrome. Indomethacin, a non-steroidal anti-inflammatory agent as well as a prostaglandin-synthetase inhibitor, partially reversed the in vitro splenic cell suppression of infected animals.
Animals↗
Sex-related immunocompetence of BALB/c mice. I. Study of immunologic responsiveness of neonatal, weanling, and young adult mice.
The responses of lymphoid cells from the thymus, lymph nodes, and spleen of male and female BALB/c mice were evaluated to determine if sex-related variations in immune expression could be found. Immunologic assays used included blastogenic responses to mitogens, mixed lymphocyte responses, and direct and indirect measurement of plaque-forming cells against soluble and particulate antigens. The results indicated that responses of spleen cells from young adult female mice were higher than those of males in all comparative tests. Little or no differences between the sexes were observed in the mitogenesis of lymph nodes and thymuses. Newborn mice did not demonstrate the sex-associated immune differences. Among the weanling mice slight differences between male and female spleen cells responsiveness to mitogenic agents were observed.
Aging↗
Quantitative differences in immune responses during the various stages of the estrous cycle in female BALB/c mice.
The immune responsiveness of spleens from female BALB/c mice to PHA, Con A, and LPS was greater at proestrus and metestrus as compared with estrus and diestrus. The peaks of responsiveness corresponded to reported elevated levels of estrogen and pregnenolone during these phases of the cycle. Similar results were obtained with the IgM or direct plaque-forming cell responses, which were also increased at proestrus and metestrus. It appears that female hormones may directly or indirectly stimulate immune responsiveness in adult mice.
Animals↗
Arteriosclerosis: is stress-induced immune suppression a risk factor?
Female Sprague-Dawley rats, purchased as retired breeders, developed arteriosclerosis that was accompanied by immune complex deposition in the arterial lesion and depressed immune responsiveness to T cell mitogens.
Animals↗
Prostaglandins and the immune response.
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Animals↗
Increase in serum IgE levels of ovalbumin-sensitized cats and the detection of elastase and collagenase activities in secretions of sensitized feline alveolar macrophages challenged in vitro.
The feline model of respiratory hypersensitivity induced by intraperitoneal injection of ovalbumin has been studied. IgE serum antibodies were present for 3-10 weeks following sensitization, with maximum titers occurring between 50 and 70 days. Similarly, peak passive cutaneous anaphylaxis reactions occurred between 50 and 70 days. Alveolar macrophages, obtained by tracheal lavage at 65 days after sensitization, produced elastase like and collagenase-like secretions 48 h after challenge with ovalbumin in culture. Macrophages from nonsensitized cats did not produce these secretions. It is hypothesized that reaginic antibodies and sensitized alveolar macrophages, such as those found in the cat model, may be responsible in part for the destruction of lung tissue found in long-term respiratory diseases, similar to fibrosing alveolitis and pulmonary emphysema in man.
Animals↗
Increase in the severity of allergic-type bronchospasm in sensitized and challenged cats treated with cortisone.
The feline model of immediate hypersensitivity to intraperitoneal ovalbumin sensitization, followed 65 days later by intravenous challenge, was used in this study to determine the effect of cortisone acetate administration on the severity of allergic bronchospasm. Cortisone acetate given intramuscularly prior to, during and immediately after sensitization increased the severity of the allergic response. Comparison of the respiratory, blood pressure and heart rate responses in cortisone-treated animals with nontreated controls indicated a significantly increased challenge reaction among the treated group. Of 7 cats receiving cortisone treatment, 5 died during the 30-min challenge monitoring period. None of the nontreated control group died. It is hypothesized that cortisone treatment impaired the activity of the cortisone-sensitive thymus-derived (T) cells.
Animals↗
Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice.
Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
Animals↗
Prostaglandin synthesis inhibition: effect on bone changes and sarcoma tumor induction in balb/c mice.
An increase in prostaglandins (PGs) of the E series has been demonstrated in Moloney sarcoma virus (MSV)-induced leg tumors of 6-week-old BALB/c male mice. The level of the hormone has been shown to increase with the tumor diameter and decrease with tumor regression. At the peak of tumor size the tibial bones of the mice were considerably deformed, suggesting osteoclastic activity. The systemic calcium level was not elevated, indicating possible release of calcium into the local tumorous area. In mice treated with indomethacin the tumors failed to develop and PG levels were markedly lower. Tibial bones of treated mice were similar in appearance to those of control, non-tumorous mice. PG levels of DBA/1J mice bearing extensive Cloudaman S91 melanomas were not elevated and no bone deformation was seen. When contrasted with studies of immuno-depressed mice the results suggest that indomethacin acted in conjunction with and possibly to restore the PG-induced depression of the immune system in preventing tumor development. It is also hypothesized that indomethacin, by suppressing the PG-mediated calcium release from bone, could be operative in inhibiting tumor growth.
Animals↗