Publications by authors named "F Lynn Sonderegger"

Background: Endothelial dysfunction might contribute to the development of leptospiral pulmonary hemorrhage syndrome (LPHS).

Hypothesis: Serum concentrations of markers of endothelial activation and dysfunction are higher in dogs with leptospirosis and correlate with the occurrence of LPHS and a higher case fatality rate.

Animals: Clinically healthy dogs (n = 31; 10/31 dogs confirmed healthy based on no detected abnormalities on blood work), dogs with leptospirosis with LPHS (n = 17) and without LPHS (n = 15), dogs with acute kidney injury not due to leptospirosis (AKI-nL, n = 34).

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Background: Osteosarcoma (OSA) in dogs is an aggressive bone tumor with frequent chemotherapy failure and translational relevance for human health.

Hypothesis/objectives: We hypothesized that dogs with OSA could be treated safely by ex vivo activated T-cells that were generated by autologous cancer vaccination and supported by interleukin-2 (IL-2) treatment with survival more than twice that reported for amputation alone.

Animals: Osteosarcoma-bearing dogs (n = 14) were enrolled in a single-arm prospective trial after complete staging before amputation.

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Viral infection of the central nervous system can result in encephalitis. About 20% of individuals who develop viral encephalitis go on to develop epilepsy. We have established an experimental model where virus infection of mice with Theiler's murine encephalomyelitis virus (TMEV) leads to acute seizures, followed by a latent period (no seizures/epileptogenesis phase) and then spontaneous recurrent seizures-epilepsy.

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T cells predominate the immune responses in the synovial fluid of patients with persistent Lyme arthritis; however, their role in Lyme disease remains poorly defined. Using a murine model of persistent Lyme arthritis, we observed that bystander activation of CD4 and CD8 T cells leads to arthritis-promoting IFN-γ, similar to the inflammatory environment seen in the synovial tissue of patients with posttreatment Lyme disease. TCR transgenic mice containing monoclonal specificity toward non- epitopes confirmed that bystander T cell activation was responsible for disease development.

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Article Synopsis
  • - The study investigates severe Lyme arthritis in C3H mice infected with Borrelia burgdorferi, focusing on the role of type I interferon (IFN) and how it contributes to the disease process.
  • - Researchers used genetically modified mice lacking the type I IFN receptor to analyze how various joint cells contribute to the IFN response, revealing that myeloid cells, endothelial cells, and fibroblasts played key roles.
  • - The findings highlight complex interactions between different cell types in the joint that trigger the IFN response, suggesting similar mechanisms could be relevant for other diseases linked to type I IFN, like lupus and certain rheumatoid arthritis forms.
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