muramidase and Shock

Type 1 diabetes in NOD mice can be prevented through autoantigen vaccination by shifting lymphocyte differentiation toward a T-helper 2 (Th(2)) response. However, in other models of autoimmunity, this approach may be accompanied by unexpected triggering of Th(2)-dependent anaphylactic shock. To test the safety of vaccination therapy in the NOD mouse model, we evaluated the effects of immunization with a wide battery of antigens in NOD, BALB/c, and C57BL/6 mice. Surprisingly, a nondiabetogenic antigen, hen egg white lysozyme, induced severe shock exclusively in NOD mice (shock in 11 of 11 mice, lethal in 3 mice). Shock severity was further increased by a more pronounced Th(2) setting generated by 1alpha,25(OH)(2)D(3) administration (17 of 17 mice, lethal in 14 mice, P < 0.0001). Pretreatment with dexamethasone resulted in full rescue, indicating an immune-mediated mechanism. Serum IgE levels and Th(1)/Th(2) cytokine profile analysis showed that the shock phenomenon was paralleled by a Th(2) response. mRNA expression of platelet-activating factor receptor (PAF-R) was significantly higher in NOD mice (P < 0.01) and was further increased by 1alpha,25(OH)(2)D(3). Pretreatment with WEB2086 (PAF-R antagonist) again protected all mice from lethal shock, indicating PAF as an anaphylaxis effector. In conclusion, in NOD mice, vaccination leading to a Th(2) immune shift can result in a lethal anaphylactic reaction.

Topics: Animals; Autoantigens; Calcitriol; Chickens; Dexamethasone; Diabetes Mellitus, Type 1; Disease Models, Animal; DNA Primers; Immunoglobulin E; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred NOD; Muramidase; Platelet Membrane Glycoproteins; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Shock; T-Lymphocytes, Helper-Inducer; Th2 Cells; Vaccines

To investigate whether vaccination could induce lethal shock and which mechanisms are involved in this phenomenon, we tested a panel of autoantigens or diabetes-irrelevant peptides or proteins in nonobese diabetic (NOD), Balb/c, and C57Bl/6 mice. Of the antigens tested, only nondiabetogenic hen egg white lysozyme induced a severe form of shock exclusively in NOD mice. The mechanism involved is suggestive of a Th(2)-mediated anaphylactic reaction possibly connected to activation of PAF and triggering of DIC.

Topics: Animals; Chickens; Egg White; Mice; Mice, Inbred C57BL; Mice, Inbred NOD; Muramidase; Shock; Vaccines

Changes of the body fluid exchange and of the composition of metabolites in the hepatosplanchnic area in canine hemorrhagic and endotoxin or septic shock models were studied by investigating the qualitative and quantitative changes in thoracic duct lymph draining from abdominal organs. In the present study, it might be summarized that the changes in the flow rate and composition of thoracic duct lymph were put forward to much more directly and apparently indicate the degree of hepatosplanchnic cellular impairment in canine experimental shock than in the circulating blood.

Topics: Animals; Dogs; Endotoxins; Escherichia coli; Intestine, Small; Lactates; Lymph; Muramidase; Serotonin; Shock; Shock, Hemorrhagic; Thoracic Duct

Topics: Anaphylaxis; Animals; Blood Chemical Analysis; Catecholamines; Chlorprothixene; Epinephrine; Lagomorpha; Muramidase; Nialamide; Norepinephrine; Ovalbumin; Prednisone; Rabbits; Research; Serotonin; Shock

Topics: Aniline Compounds; Bacteria; Cold Temperature; Deoxyribonucleases; DNA; Enterobacter aerogenes; Magnesium; Metabolism; Muramidase; Naphthalenes; Pepsin A; Pharmacology; Research; Ribonucleases; RNA; RNA, Bacterial; Shock; Sucrose; Trypsin

Topics: Animals; Hemorrhage; Lagomorpha; Muramidase; Rabbits; Shock; Shock, Hemorrhagic

Topics: Equipment Failure; General Adaptation Syndrome; Humans; Muramidase; Shock