Michael Laiosa, PhD
Assistant Professor
Education
PhD, State University of New York, Upstate Medical University, Microbiology and Immunology, 2002
B.S., State University of New York at Geneseo, Biochemistry, 1997
Interests & Expertise
Understanding why the prevalence of childhood diseases of the immune system such as leukemia, autoimmunity, and atopy are all on the rise in recent decades. Long-term research plans are centered on translating how early life exposures adversely affect immune system development and function later in life with specific emphasis on:
- Identifying developmental/early life environmental factors which influence cancer risks and autoimmune pathogenesis.
- Identifying pre- and early post-natal chemopreventative agents which may reduce risk for developing diseases such as leukemia, atopy, and autoimmune disease.
- Determine the impact of early life exposures to chemical mixtures on long term immunological health outcomes.
Teaching & Research Statement
The primary research objectives in my laboratory are focused on understanding why the prevalence of childhood diseases of the immune system such as leukemia, autoimmunity, and atopy are all on the rise in recent decades. One explanation comes from a growing body of evidence suggesting that environmental exposures occurring in the mother's womb, interact with genetic susceptibility factors in the developing child. These gene-environment interactions cause functional changes during development of the immune system potentially leading to later life diseases. Consequently, understanding mechanisms by which early life immune insults increase the risk for developing childhood and even adult diseases represents a potentially rich area for improving public health by developing novel prevention and treatment strategies.
To begin addressing these childhood public health concerns, one of the first projects my laboratory is developing is designed to better understand potential links between environmental exposures and childhood leukemia. Specifically, the laboratory will test the hypothesis that pre- and early post-natal activation of the ligand activated Aryl hydrocarbon receptor (AHR) by the ubiquitous environmental pollutant dioxin, (also known as TCDD), interacts with a common leukemia genetic risk factor promoting T-cell acute lymphoblastic leukemeogenesis. The proposal also tests whether leukemeogenesis can be mitigated by using natural AHR antagonists such as resveratrol (from red wine).
Representative Publications
Farrer DF, Eckles KE, Hueber SM, Laiosa MD, and McCabe, MJ. (2008). The heavy metal lead, disrupts a myeloid suppressor cell-dependent inhibition of alloreactive CD4+ T cell proliferation by targeting inducible nitric oxide synthase. Toxicology and Applied Pharmacology, 229:135-45.
Laiosa MD, Eckles KE, Langdon M, Rosenspire AJ, and McCabe MJ. (2007). Exposure to inorganic mercury in vivo attenuates extrinsic apoptotic signaling in Staphylococcal aureus enterotoxin B stimulated T-cells. Toxicology and Applied Pharmacology, 225:229-336.
Laiosa MD. (2005). The effect of steroid hormones on the immune system. In The Encyclopedic Reference of Immunotoxicology. Vohr, HW, editor. Springer, Heidelberg, Germany. 1st Edition: 603-8.
Laiosa MD, Wyman A, Murante FG, Gasiewicz TA, Silverstone AE. (2003). Cell proliferation arrest within intrathymic lymphocyte progenitor cells causes thymic atrophy mediated by the aryl hydrocarbon receptor. The Journal of Immunology, 171:4582-91.
Laiosa MD, Lai ZW, Thurmond TS, Fiore NC, Gasiewicz TA, Silverstone AE. (2001). 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin causes alterations in lyphocyte development and thymic atropy in hemopoietic chimeras generated from mice deficient in ARNT2. Toxicological Sciences, 69:117-24.
Active Grants
Environmental Influence on T-Cell Leukemia: Role of Notch and AhR Signaling, 2008-2013, 1K99ES016586-01