My approach to research and teaching reflects my own background -- I've lived and worked in several countries and am a passionate advocate for travel, adventure and cultural exchange. My core philosophy is an extension of this experience where I believe the purpose of science is to serve and better humanity. This collective service has the potential to improve health, welfare and our environment. I apply this approach by trying to make our research experience fun, supportive, collaborative and social.
I graduated with a Bachelor of Science in Microbiology from Colorado State University. While at Colorado State, I trained in the Mycobacterial Research Labs, an internationally recognized centre for investigation of mycobacterial diseases and pathogens. At Colorado State, I developed what would become a life-long interest in the taxonomic family of Mycobacteriaceae, which contains a range of notable human and animal pathogens, including the causative agent for Tuberculosis. Following this, I worked for a veterinary biotech company and then moved into commercial research and development for a small biotech instrumentation company. In 2002, I relocated to the Trudeau Institute, a private research organization focusing on pulmonary pathogens, to continue my work with models of Tuberculosis and other mycobacterial pathogens. While at the Trudeau Institute, I earned a Ph.D. from the University of Porto in Portugal with a mechanistic focus on how infection with Mycobacterium avium modulates host immunity.
Before moving to Leicester, I held two academic appointments where I taught environmental microbiology and medical microbiology. During this formative period, I developed my approach to teaching which leverages the student's interests and experiences to enhance engagement.
In my work in Leicester, I'm an advocate of research-focused teaching where I believe that the best science arises from a highly diverse and international group of students who become invested in the scientific endeavour through working in a lab and participating in research. In this regard, we emphasize hypothesis development, experimental design and formal hypothesis testing which culminates in various forms of scientific communication. Simply stated, for a student to succeed and to maximize their potential, every student needs to be able to bring their whole self to work.
Science is social and science is fun!
1. PHOSP-COVID Collaborative Group, Clinical characteristics with inflammation profiling of long COVID and association with 1-year recovery following hospitalisation in the UK: a prospective observational study. Lancet Respir Med, 2022.
2. Sulman, S., et al., Balance between Protection and Pathogenic Response to Aerosol Challenge with Mycobacterium tuberculosis (Mtb) in Mice Vaccinated with TriFu64, a Fusion Consisting of Three Mtb Antigens. Vaccines (Basel), 2021. 9(5).
3. Evans, R.A., et al., Physical, cognitive, and mental health impacts of COVID-19 after hospitalisation (PHOSP-COVID): a UK multicentre, prospective cohort study. Lancet Respir Med, 2021. 9(11): p. 1275-1287.
4. Pearl, J.E., M. Das, and A.M. Cooper, Immunological roulette: Luck or something more? Considering the connections between host and environment in TB. Cell Mol Immunol, 2018. 15(3): p. 226-232.
5. Torrado, E., et al., Interleukin 27R regulates CD4+ T cell phenotype and impacts protective immunity during Mycobacterium tuberculosis infection. The Journal of experimental medicine, 2015. 212(9): p. 1449-63.
6. Pearl, J.E., Free Radicals in Mycobacterial Disease, in Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2. 2015, American Chemical Society. p. 503-539.
7. Torrado, E., et al., Differential and site specific impact of B cells in the protective immune response to Mycobacterium tuberculosis in the mouse. PloS one, 2013. 8(4): p. e61681.
8. Pearl, J.E., et al., Nitric oxide inhibits the accumulation of CD4+CD44hiTbet+CD69lo T cells in mycobacterial infection. European journal of immunology, 2012. 42(12): p. 3267-79.
9. Khader, S.A., et al., IL-23 is required for long-term control of Mycobacterium tuberculosis and B cell follicle formation in the infected lung. Journal of immunology, 2011. 187(10): p. 5402-7.
10. Robinson, R.T., et al., Mycobacterium tuberculosis infection induces il12rb1 splicing to generate a novel IL-12Rbeta1 isoform that enhances DC migration. The Journal of experimental medicine, 2010. 207(3): p. 591-605.
11. Khader, S.A., et al., In a murine tuberculosis model, the absence of homeostatic chemokines delays granuloma formation and protective immunity. Journal of immunology, 2009. 183(12): p. 8004-14.
12. Reiley, W.W., et al., ESAT-6-specific CD4 T cell responses to aerosol Mycobacterium tuberculosis infection are initiated in the mediastinal lymph nodes. Proceedings of the National Academy of Sciences of the United States of America, 2008. 105(31): p. 10961-6.
13. Mayer, K.D., et al., Cutting edge: T-bet and IL-27R are critical for in vivo IFN-gamma production by CD8 T cells during infection. Journal of immunology, 2008. 180(2): p. 693-7.
14. Khader, S.A., et al., IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge. Nature immunology, 2007. 8(4): p. 369-77.
15. Khader, S.A., et al., Interleukin 12p40 is required for dendritic cell migration and T cell priming after Mycobacterium tuberculosis infection. The Journal of experimental medicine, 2006. 203(7): p. 1805-15.
16. Cruz, A., et al., Cutting edge: IFN-gamma regulates the induction and expansion of IL-17-producing CD4 T cells during mycobacterial infection. Journal of immunology, 2006. 177(3): p. 1416-20.
17. Khader, S.A., et al., IL-23 compensates for the absence of IL-12p70 and is essential for the IL-17 response during tuberculosis but is dispensable for protection and antigen-specific IFN-gamma responses if IL-12p70 is available. Journal of immunology, 2005. 175(2): p. 788-95.
18. Florido, M., et al., Gamma interferon-induced T-cell loss in virulent Mycobacterium avium infection. Infection and immunity, 2005. 73(6): p. 3577-86.
19. Pearl, J.E., et al., IL-27 signaling compromises control of bacterial growth in mycobacteria-infected mice. Journal of immunology, 2004. 173(12): p. 7490-6.
20. König, S., et al., Protein Expression Analysis, in Analysing Gene Expression. 2004, Wiley-VCH Verlag GmbH & Co. KGaA. p. 623-702.
21. Hancock, W.W., et al., Intact type 1 immunity and immune-associated coagulative responses in mice lacking IFN gamma-inducible fibrinogen-like protein 2. Proceedings of the National Academy of Sciences of the United States of America, 2004. 101(9): p. 3005-10.
22. Turner, J., et al., CD8- and CD95/95L-dependent mechanisms of resistance in mice with chronic pulmonary tuberculosis. American journal of respiratory cell and molecular biology, 2001. 24(2): p. 203-9.
23. Pearl, J.E., et al., Inflammation and lymphocyte activation during mycobacterial infection in the interferon-gamma-deficient mouse. Cellular immunology, 2001. 211(1): p. 43-50.
24. Pearl, J.E., I.M. Orme, and A.M. Cooper, CD95 signaling is not required for the down regulation of cellular responses to systemic Mycobacterium tuberculosis infection. Tubercle and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease, 2000. 80(6): p. 273-9.
25. Cooper, A.M., et al., Expression of the nitric oxide synthase 2 gene is not essential for early control of Mycobacterium tuberculosis in the murine lung. Infection and immunity, 2000. 68(12): p. 6879-82.
Based on my publication record and current research I’m an expert in non-tuberculous mycobacteria.