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Inflammation


Inflammation, a complex pathophysiological process, plays an important role in numerous responses to pathogens and stimuli in the animal body, and it is central to many diseases including cardiovascular diseases, colitis, arthritis and dermatitis. In addition, inflammation plays a crucial role in the microenvironment of tumors where inflammatory signals mediate the proliferation, survival and migration of cancer cells.

Due to these diverse roles of inflammation in such a wide array of diseases, identifying novel targets in inflammatory signaling cascades and understanding how inflammatory mediators contribute to disease development is a major biomedical research goal that will support the development of novel anti-inflammatory drugs. 

Using a variety of state-of-the-art cellular, molecular, genetic, pharmacological and imaging approaches, members of the department study various aspects of inflammation including its role in the tumor microenvironment and the signaling mechanisms induced by pro-inflammatory cytokines.

Members of the Department of Animal Biology who study inflammation also contribute to and collaborate with various centers and research institutes, including the Mari Lowe Center for Comparative Oncology.

Focus: Dr. Serge Fuchs

Dr. Serge Fuchs, Penn Vet 

The Fuchs lab studies mechanisms that regulate the sensitivity of animal cells to a type of anti-viral cytokines, type I interferons, which play an important role in immunomodulation and tumorigenesis.

Faculty


  • Dr. Ellen Puré
    • Inflammatory and fibrotic responses are complex and highly orchestrated reactions to disruptions in homeostasis, stress stimuli and infection. Our studies focus on sterile inflammation, inflammatory and fibrotic responses that occur in the absence of infection.  Typically such responses are self-limiting, waning as the insult resolves and active regulatory mechanisms are engaged.
    • Notably, many diseases, including cardiovascular disease, tissue fibrosis and scarring, cancer and obesity are associated with chronic inflammation that results from either a persistent insult or a dysfunction in resolution. Studies in our lab focus on defining initiators of sterile inflammation, and determining the roles of stromal cells (such as fibroblasts) and extracellular matrix in sterile inflammation. By defining the molecular mechanisms that promote chronic inflammation and fibrosis and or are involved in the resolution of inflammation and fibrosis, we hope to identify therapeutic targets for improved treatment of cardiovascular disease, tissue fibrosis and cancer.
  • Dr. Serge Fuchs
    • Our lab studies mechanisms that regulate the sensitivity of animal cells to a type of anti-viral cytokines, type I interferons, which play an important role in fuch6121immunomodulation and tumorigenesis.
    • Specifically, we have delineated critical mechanisms that govern the downregulation of the receptors of those cytokines, and have found that failure to stimulate downregulation of those receptors can lead to increased tissue damage, prolonged inflammation and impaired ability of tissues to regenerate.
    • We continue to investigate the mechanisms underlying the role of type I interferons and their receptors and seek to develop pharmacologic agents for preventative downregulation of the receptors to relieve tissue damage and promote regeneration.
  • Dr. Michael May
    • Our lab focuses on understanding the mechanisms that regulate activation of the inducible transcription factor NF-ĸB, which is crucial for a wide range of cellular functions in innate and adaptive immunity and lymphocyte development.
    • Aberrant NF-κB activationoccurs in chronic inflammatory diseases including atherosclerosis and rheumatoid arthritis, and dysregulated NF-κB signaling is a hallmark of many cancers including solid tumors, leukemias and lymphomas.
    • We work to identify the mechanisms of activation in order to define novel targets for therapeutic intervention, and our lab has identified a novel interaction between key proteins controlling NF-ĸB and a previously unknown signaling intermediate in lymphocyte activation named Homer 3 as well as novel mechanisms of cross talk between the major NF-ĸB signaling pathways.
    • Ongoing research includes defining the mechanisms of NF-ĸB activation and function in vascular endothelial cells that line the walls of blood vessels.