Summary: Our lab is interested in how exposure to environmental contaminants affects the immune system. Specifically, we use asbestos exposure as a model of environment-induced autoimmunity. Asbestos is a general term applied to a group of mineral fibers. Asbestos exposure can occur through commercial use (usually to chrysotile fibers) or through exposure to natural asbestos outcroppings; the latter typically occurs when people recreate or with new construction projects that disturb the minerals. Asbestos exposures are often associated with pulmonary disease, including lung cancer, interstitial fibrosis, and mesothelioma. However, we have found that exposure to amphibole asbestos (a straight-chained fiber) is also linked to an increased incidence of pleural fibrosis, systemic autoimmune disease, and increased production of autoantibodies.

The overall goals for our lab include: 1) examining how amphibole fibers alter immune responses, 2) identify cell targets for asbestos-induced autoantibodies, and 3) test therapeutics to reduce immune responses and fibrosis following asbestos exposure.

Minimum classes:
Cell biology or Microbiology (required)
Immunology (optional)
Molecular biology (optional)
A&P (optional)

1) Neutrophils are some of the first immune cells to respond to infection. Similarly, they are some of the first cells recruited to sites of asbestos deposition. Therefore, we are interested in understanding how asbestos fibers affect these cells and in turn how these effects may alter immune responses to fibers. The fellow working on this project will use techniques like cell culture, microscopy, and flow cytometry to determine the mechanisms of neutrophil response to asbestos fibers.

2) B cells are part of the adaptive immune system and implicated in the development of autoimmune disease through production of autoantibodies. We suspect that asbestos fiber exposure can change the function or differentiation of B cells into different subsets. This project aims to identify B cell responses to asbestos fibers and to measure B cell responses following exposures by using cell culture, flow cytometry, and animal models.

3) We have previously reported that a synthetic lignan, LGM2605, reduces early immune responses to asbestos exposure. An on-going lab project is to characterize both innate and adaptive immune responses following LGM2605 treatment and to determine if this compound can reduce asbestos-associated fibrosis and autoimmune disease. The fellow working on this project will learn histology, microscopy, ELISA, and flow cytometry techniques.

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