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Biomedical subjects

M N Kwasniewski

Publications and source records attributed to M N Kwasniewski.

7 recordsLinked to original sources
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↗
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↗
PubMed1988

Induction of continuous I-A expression by murine peritoneal macrophages: lack of correlation with T cell responses of Bcgr and Bcgs mice.

The induction of continuous I-A expression by L3T4 and Lyt2 lymphocyte subpopulations from Bcgr and Bcgs mice was compared. We found that the induction of continuous I-A expression was independent of the Bcg genotype of the T cells. T cells from congenic Bcgs BALB/c mice and C.D2Bcgr mice could not induce continuous I-A expression in vitro and were deficient in their ability to produce IFN-gamma in vitro. In contrast, T cells from other strains of Bcgr and Bcgs mice could induce continuous I-A expression. Both recombinant IL-2 and IL-4 acted synergistically with low levels of IFN-gamma to induce continuous I-A expression by macrophages from Bcgr mice.

Animals↗