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A Stelzner

Publications and source records attributed to A Stelzner.

159 records · Page 9Linked to original sources
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6-Sulfanilamidoindazole arthritis of the rat: complement activity and sulfhydryl group concentration of the serum in three different phases of inflammation.

In 6-sulfanilamidoindazole (6-SAI) arthritis the total haemolytic complement activity of the serum was significantly increased by 69% in developing arthritis at day 4, and by 42% in fully developed arthritis at day 8. In declining arthritis at day 12, 5 days after the last administration of the prophlogistic agent 6-SAI, no difference of the serum complement activity between arthritic rats and non-arthritic controls could be determined. The serum SH group concentration was significantly decreased by 31% at day 4 and by 54% at day 8, but it was nearly normalized at day 12. There was no close correlation between increase of paw diameter and serum complement activity in 6-SAI-arthritic rats. It is suggested that investigations on the role that complement components might play in 6-SAI arthritis could be interest.

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Coxsackievirus B3-induced myocarditis in MHC class II-deficient mice.

OBJECTIVES: The pathogenesis of coxsackievirus B3 (CVB3)-induced myocarditis was investigated in immunocompetent C57BL/6 and MHC class II knockout mice with identical genetic backgrounds. STUDY DESIGN/METHODS: We analyzed the histology and immunohistology of myocardial injury, the replicating virus titer, and antibody response in the early and late phase of disease. RESULTS: CVB3-infected C57BL/6 mice showed acute myocarditis, with spontaneous healing, virus elimination, anti-CVB3 IgM/IgG production, and neutralizing antibody response. In contrast, MHC class II knockout mice developed less severe acute myocarditis, persistence of infiltrations and strong fibrosis, virus persistence, and weak IgG response, with absence of virus neutralizing antibodies. CONCLUSIONS: Immunodeficient organisms are more susceptible to long-term heart muscle injuries after infection with CVB3. The presence of CD4+ T cells are necessary to prevent the development of chronic disease.

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PubMedDate not supplied

Coxsackievirus B3-induced chronic myocarditis in outbred NMRI mice.

OBJECTIVES: The pathogenesis of coxsackievirus B3 (CVB3)-induced myocarditis was investigated in adult Han:NMRI mice. The outbred model, in comparison with inbred models, represents better the natural variable susceptibility of the human population. STUDY DESIGN/METHODS: We analyzed the replicating virus titer, the antibody response in the acute and chronic phase of disease, the histology of myocardial injury, and the persistence of viral RNA. RESULTS: NMRI mice infected with 5000 plaque-forming units (PFU) of the CVB3 variant "P"D, a lytic variant to human fibroblast lines, showed a peak of virus replication at day 14 and developed a severe acute myocarditis. The chronic myocarditis was characterized by progressive fibrosis, small foci of infiltrates, persistent viral RNA in the heart, and detectable anti-CVB3 IgG production and neutralizing antibody response up to day 98 postinfection. CONCLUSIONS: CVB3"P"D is able to induce chronic myocarditis in NMRI mice. This model provides a method for examining and proving the mechanisms of myocardial pathogenesis and of developing therapeutic strategies.

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