Targeting Tick-Borne Diseases - Day 1 - Cambridge Healthtech Institute

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Wednesday, October 29

1:00 pm Registration


2:00 Welcome Remarks by Session Chairperson

Konstance Knox, Ph.D., CEO, Coppe Healthcare Solutions, Inc.

2:10 Post-Treatment Lyme Disease Syndrome: Development of a Case Definition and Future Biomarkers

John N. Aucott, Ph.D., Department of Medicine, The Johns Hopkins University School of Medicine

Post-Treatment Lyme Disease Syndrome (PTLDS) can be defined in patients who have prolonged symptoms after antibiotic treatment of Lyme disease. Diagnosis of PTLDS is made on the basis of the patient’s past history and current symptoms. Self-administered standardized instruments can be used to quantify symptoms and their impact on health-related function. Biorepositories of blood samples from patients with well characterized PTLDS are essential to develop future biomarkers for PTLDS.

2:40 Bacteria and Viral Co-Infections in Wisconsin Tick Population

Konstance Knox, Ph.D., CEO, Coppe Healthcare Solutions, Inc.

Coppe Healthcare Solutions investigated bacteria and viral co-infections in I. scapularis and D. variabilis ticks collected by the Wisconsin Department of Natural Resources. Ticks collected from the geographic survey underwent testing for the presence of Borrelia burgdorferi, Anaplasma monocytophilium, Babesia microti and Powassan/Deer Tick virus. Individual ticks were shown to harbor multiple bacterial or bacterial plus viral agents. These findings document that the Wisconsin tick population includes ticks that harbor one or more infectious agents, and we hypothesize that a questing tick could transmit one or more agents during a single blood meal.

3:10 The Human Immune Response in Lyme Borreliosis

Mark J. Soloski, Ph.D., Professor of Medicine, Division of Rheumatology; Director, Immunology Training Program, Johns Hopkins School of Medicine

We have applied proteomic, genomic and immune cell profiling approaches toward understanding the immune pathways activated during acute human Lyme disease and following antibiotic treatment. These studies, while identifying a Lyme disease signature, found that the host response triggered during infection has considerable heterogeneity. These results will be presented and discussed in the context of reaching a mechanistic understanding of the range of pathophysiological responses to Borrelia burgdorferi.

3:40 Refreshment Break with Exhibit and Poster Viewing

4:20 Lysosomal β-Glucuronidase Regulates Lyme and Rheumatoid Arthritis Severity

Cory Teuscher, Ph.D., Teuscher Laboratory, University of Vermont

The spectrum of Lyme disease severity among infected patients suggests that host genetics contribute to pathogenic outcomes, particularly in patients who develop arthritis. Using a forward genetics approach, we identified the lysosomal enzyme β-glucuronidase (GUSB), a member of a large family of co-regulated lysosomal enzymes, as a key regulator of Lyme-associated arthritis severity. Severely arthritic C3H mice possessed a naturally occurring hypomorphic allele, Gusbh. C57BL/6 mice congenic for the C3H Gusb allele were prone to increased Lyme-associated arthritis severity. C3H mice expressing WT Gusb as a transgene were protected from severe Lyme arthritis. Importantly, the Gusbh allele also exacerbated disease in a serum transfer model of rheumatoid arthritis. Development of Lyme and rheumatoid arthritis in Gusbh-expressing mice was associated with heightened accumulation of GAGs in joint tissue. We propose that GUSB modulates arthritis pathogenesis by preventing accumulation of proinflammatory GAGs within inflamed joint tissue, a trait that may be shared by other lysosomal exoglycosidases.

4:50 Role of Eicosanoids in Experimental Lyme Disease

Charles R. Brown, Ph.D., Professor, Department of Veterinary Pathobiology, University of Missouri-Columbia

Experimental Lyme arthritis is an inflammatory arthritis caused by infection of mice with the spirochete, Borrelia burgdorferi. It recapitulates many of the disease parameters seen in human patients with Lyme arthritis, and thus serves as a model system for the investigation of disease pathogenesis. While much progress has been made in defining components of the immune response to Borrelia infection, an overall understanding of the host response leading to arthritis resistance or susceptibility remains elusive. In this review, we will focus on recent advancements of our understanding of the roles of eicosanoids as inflammatory mediators in the regulation of experimental Lyme arthritis. Eicosanoids, such as PGE2 and LTB4, are powerful regulators of inflammatory responses and thus may be important mediators of Lyme arthritis.

5:20 Welcome Reception with Exhibit and Poster Viewing

6:20 Close of Day

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