Jennifer Nyland, PhD:
Johns Hopkins Bloomberg School of Public Health
Ph.D. State University of New York Upstate Medical University
B.A. Cornell University
My research interests include translational research on the relationship between environmental toxicants and autoimmune disease. We have utilized an animal (mouse) model of autoimmune heart disease to study mechanisms of mercury-induced exacerbation of innate immune responses. We have utilized in vitro techniques to study mercury-induced changes in the response of human immune cells in terms of their cytokine production. We have used epidemiological methods to evaluate the relationship between mercury exposure (inorganic mercury via occupational exposure or methyl mercury through contaminated fish consumption) and biomarkers of autoimmune dysfunction. Beyond mercury, we have examined the impact of exposure to nanoparticles in vitro on cells of the immune system.
Mercury is a ubiquitous global contaminant with a range of toxic properties including neurotoxic (usually occurring at high exposures) and immunotoxic (usually occurring at lower range exposures) effects. Individuals are primarily exposed to low levels of mercury through either occupational routes (mercury is used in some electronics and light fixtures, in dental amalgams, among other applications) or contaminated fish consumption (generally large fish-eating fish have the highest levels of mercury). We hypothesize that certain individuals are more sensitive or susceptible to mercury-induced immunotoxicity. For these individuals, exposure to mercury might increase their likelihood to develop an autoimmune disease or increase the severity of a pre-existing autoimmune disease. We do not imagine that low level mercury exposure alone can induce disease, however, in the presence of other environmental factors (such as viral infection as we use in some of our animal models), mercury could act synergistically to push a susceptible individual down a deleterious path toward disease. The overall goal, therefore, of research in my lab is to identify characteristics of these susceptible individuals that would make their immune system more likely to respond to the immunotoxic properties of low level mercury exposure.
- Nyland, JF, SB Wang, DL Shirley, EO Santos, AM Ventura, J deSouza, and EK Silbergeld. 2011. Fetal and maternal immune responses to methyl mercury exposure: a cross-sectional study. Environ Res. 111(4): 584-589.
- Gardner, RM, JF Nyland, and EK Silbergeld. 2010. Differential immunotoxic effects of inorganic and organic mercury species in vitro. Tox Letters. 198: 182-190.
- Gardner, RM, JF Nyland, IA Silva, AM Ventura, JM deSouza, and EK Silbergeld. 2010. Mercury exposure, serum antinuclear/ antinucleolar autoantibodies, and serum cytokine levels in mining populations in Amazonian Brazil: a cross-sectional study. Environ Res. 104(4): 345-354.
- Feng, F, J Nyland, M Banyai, A Tatum, AE Silverstone, and J Gavalchin. 2010. The induction of the lupus phenotype by estrogen is via an estrogen receptor-α-dependent pathway. Clinical Immunology. 134: 226-236.
- Gardner, RM, JF Nyland, SL Evans, S Wang, KM Doyle, CM Crainiceanu, and EK Silbergeld. 2009. Mercury induces an unopposed inflammatory response in human peripheral blood mononuclear cells in vitro. Environ Health Persp. 117: 1932-1938.
- Nyland, JF, JKJ Bai, HE Katz, and EK Silbergeld. 2009. In vitro interactions between splenocytes and dansylamide dye-embedded nanomaterials detected by flow cytometry. Nanomedicine: NBM. 5: 298-304.
- Nyland, JF and EK Silbergeld. 2009. A nanobiological approach to nanotoxicology. Hum Exp Toxicol. 28:393-400.
- Frisancho-Kiss, S, SE Davis, JF Nyland, JA Frisancho, D Cihakova, MA Barrett, NR Rose, and D Fairweather. 2007. Cutting Edge: Cross-regulation between TLR4 and T cell Ig mucin-3 determines sex differences in inflammatory heart disease. J Immunol. 178: 6710-6714.
- Frisancho-Kiss, S, JF Nyland, SE Davis, JA Frisancho, MA Barrett, NR Rose, and D Fairweather. 2006. Sex differences in the immune response to Coxsackievirus B3 infection determine the severity of inflammatory heart disease in BALB/c mice. Br Research. 1126: 139-147.
- Frisancho-Kiss, S, JF Nyland, SE Davis, MA Barrett, SJL Gatewood, DB Njoku, D Cihakova, EK Silbergeld, NR Rose, and D Fairweather. 2006. Cutting Edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity. J Immunol. 176(11): 6411-6415.
- Fairweather, D, S Frisancho-Kiss, DB Njoku, JF Nyland, Z Kaya, SA Yusung, SE Davis, MA Barrett, and NR Rose. 2006. Complement receptor 1 and 2 deficiency increases coxsackievirus B3-induced myocarditis and heart failure by increasing macrophages, IL-1β and immune complex deposition in the heart. J Immunol. 176(7): 3516-3524.
- Silbergeld, EK, IA Silva, and JF Nyland. 2005. Mercury and autoimmunity: implications for occupational and environmental health. Toxicol Appl Pharmacol 207: S282-S292.
- Silva, IA, J Graber, JF Nyland, and EK Silbergeld. 2005. In vitro HgCl2 exposure of immune cells at different stages of maturation: phenotype & function. Environ Res 98: 341-348.
- Silva, IA, JF Nyland, A Gorman, A Perisse, AM Ventura, ECO Santos, JM de Souza, CL Burek, NR Rose, and EK Silbergeld. 2004. Mercury exposure, malaria, and serum antinuclear/antinucleolar antibodies in amazon populations in Brazil: a cross-sectional study. Environ Health 3(1): 11-22.
Additional Information can be found here on a personal Web page