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Biomedical subjects

E Chelmicka-Schorr

Publications and source records attributed to E Chelmicka-Schorr.

At least 19 recordsLinked to original sources
PubMed1998

Immunoaugmenting effect of FK 506 on experimental allergic encephalomyelitis in Lewis rats.

The effect of the immunosuppressive drug FK 506 on encephalomyelitis (EAE) in Lewis rats was studied. Treatment that began during EAE induction delayed EAE onset, but when the disease started it was chronic/progressive and of unusual severity and duration, leading to death in many animals. Treatment started after onset of EAE shortened the disease. Forty seven days after immunization, extensive demyelination and inflammation were observed in the spinal cords of rats treated with FK 506 from the day of EAE induction. Rats treated after EAE onset had only minimal pathological abnormalities.

Administration, Oral↗
PubMed1995

Beta-adrenergic agonists suppress chronic/relapsing experimental allergic encephalomyelitis (CREAE) in Lewis rats.

Chronic/relapsing experimental allergic encephalomyelitis (CREAE) serves as an animal model for relapsing/remitting multiple sclerosis. Treatment with the beta-adrenergic agonist isoproterenol or the beta 2-adrenergic agonist terbutaline significantly suppressed both the first acute attack and the number of relapses in CREAE Lewis rats. The number of relapses was decreased even when treatment with beta-adrenergic agonist was started after the onset of the first acute attack of CREAE. beta-adrenergic receptor number was increased significantly on splenocytes from CREAE rats as compared to healthy controls or CFA-injected rats. Terbutaline treatment of CREAE rats lowered the splenocyte receptor number to normal values.

Adrenergic beta-Agonists↗
PubMed1995

Experimental allergic encephalomyelitis, beta-adrenergic receptors and interferon gamma-secreting cells in beta-adrenergic agonist-treated rats.

Treatment with the beta 2-adrenergic agonist terbutaline or the beta-adrenergic agonist isoproterenol suppresses experimental allergic encephalomyelitis, decreases the number of IFN gamma-producing splenic cells, and decreases the number of beta-adrenergic receptors on splenic lymphocytes in Lewis rats. The effects of terbutaline are greater when the drug is given from the day of immunization through the acute phase of the illness or from day 15 postimmunization until recovery, than when given for the first 12 days after immunization.

Adrenergic beta-Agonists↗
PubMed1994

The beta 2-adrenergic agonist terbutaline suppresses experimental allergic neuritis in Lewis rats.

Treatment of rats with experimental allergic neuritis with the beta 2-adrenergic agonist terbutaline suppresses clinical symptoms, decreases demyelination and Wallerian degeneration in peripheral nerves and improves electrophysiological parameters. Treatment is highly effective when given from the time of immunization through the acute phase of illness, when given for the first 12 days after immunization and also when given after the onset of the disease.

Action Potentials↗
PubMed1993

The beta 2-adrenergic agonist terbutaline suppresses acute passive transfer experimental autoimmune myasthenia gravis (EAMG).

Treatment of Lewis rats with the beta 2-adrenergic agonist terbutaline suppressed clinical symptoms of acute passive transfer EAMG induced with monoclonal anti-acetylcholine receptor antibody and accelerated clinical recovery in affected animals. Electrophysiological studies showed that the amplitude of the first compound muscle action potential was significantly larger in terbutaline-treated rats as compared to controls. In both groups, a comparable number of inflammatory cells at the muscle endplates was seen.

Acute Disease↗
PubMed1992

Sympathectomy augments adoptively transferred experimental allergic encephalomyelitis.

Adoptively transferred experimental allergic encephalomyelitis (EAE) was significantly augmented in Lewis rats with ablated sympathetic nervous system. Sympathectomy was obtained by treatment of newborn rats with 6-hydroxydopamine. Sham-injected rats were used as a control. EAE was elicited in 7-8-week-old donor Lewis rats by immunization with a suspension of guinea pig (GP) brain and spinal cord in complete Freund's adjuvant. Successful transfer of EAE was accomplished with 50 x 10(6) lymph node cells (LNC)/rat, incubated for 72 h with GP myelin basic protein. LNC were obtained from draining lymph nodes, 9 days after immunization for EAE. The severity of passively transferred EAE was significantly augmented when donor LNC obtained from normal Lewis rats immunized for EAE were injected into sympathectomized rats as compared to sham-injected rats. When LNC were obtained from sympathectomized or sham-injected donors, the disease was significantly more severe in recipients of cells from sympathectomized animals. The severity of histological lesions in the brain and spinal cord was greater in rats with passively transferred EAE which received LNC from sympathectomized donors.

Animals↗
PubMed1992

Sympathetic nervous system modulates macrophage function.

We have reported previously that sympathectomy augments immune responses in mice and rats. In the present study, we show that ablation of the sympathetic nervous system augments macrophage function as measured by increased TNF secretion. We also show that a factor present in the sympathetic ganglia of newborn rats, suppresses secretion of TNF by LPS-stimulated macrophages as does the beta-adrenergic agonist isoproterenol.

Animals↗
PubMed1990

Sympathetic nervous system and PC12 pheochromocytoma-derived factors suppress stimulation of lymphocytes.

We have reported previously that ablation of the sympathetic nervous system augments immune responses in mice and rats. In the present study we show that a factor present in the sympathetic cervical ganglia of newborn rats suppresses Con A-induced stimulation of splenic T lymphocytes significantly whether added prior to, throughout, or following exposure to Con A. We also show that rat PC 12 pheochromocytoma cells secrete a factor which has the same inhibitory effect on T cell proliferation as the sympathetic ganglia-derived factor.

Animals↗
PubMed1989

The beta-adrenergic agonist isoproterenol suppresses experimental allergic encephalomyelitis in Lewis rats.

Treatment with the beta-adrenergic agonist isoproterenol suppresses clinical and histological experimental allergic encephalomyelitis in Lewis rats. The effect of isoproterenol treatment is greater when the drug is given from the time of immunization through the acute phase of the illness or from 8 to 14 days post-immunization than when given for the first 7 days after immunization.

Adrenergic beta-Agonists↗
PubMed1989

PC12 pheochromocytoma and sympathetic nervous system derived trophic factors augment growth of neuroblastoma.

A trophic factor secreted by PC12 rat pheochromocytoma augments growth of C1300 neuroblastoma clonal lines S20, N18 and C46, but does not affect growth of the NIE 115 line. A trophic factor present in newborn sympathetic ganglia has the same biological effect on neuroblastoma cell lines. PC12 cells and sympathetic ganglia are both of neural crest origin; possibly both secrete the same trophic factor.

Adrenal Gland Neoplasms↗
PubMed1989

The effect of chemical sympathectomy on natural killer cells in mice.

The nervous system affects immune regulation. We permanently ablated the sympathetic nervous system (SNS) of CBA mice with 6-OHDA at birth. Function of splenic natural killer (NK) cells in the sympathectomized mice was equivalent to controls at 2 weeks, but rose significantly above control levels at 4 weeks. NK cell function decreased below control values thereafter. NK cell numbers paralleled these changes in NK cell function. Our data suggest that the SNS may regulate the number and function of splenic NK cells during development.

Aging↗