TY - GEN
T1 - In Silico Model of Vitamin D3 Dependent NADPH Oxidase Complex Activation during Mycobacterium Infection
AU - Gough, Maya
AU - May, Elebeoba
N1 - Funding Information:
Research supported in part by UH-HMRI GRF in Clinical & Translational Research, DTRA award # FA8650-10-2-6062 subaward#2381, NSF BIO/MCB Award #1445470, UH-HEALTH Research Institute Maya Gough is a Ph. D. candidate in the Department of Biomedical Engineering at the University of Houston, Houston TX 77204-5060 USA (e-mail: megough@central.uh.edu). Elebeoba E. May is an Associate Professor in the Department of Biomedical Engineering at the University of Houston, Houston TX 77204-5060 USA. *Corresponding author (phone: 713-743-3851; fax: 713-743-0226; e-mail: eemay@central.uh.edu).
Publisher Copyright:
© 2018 IEEE.
PY - 2018/10/26
Y1 - 2018/10/26
N2 - Mycobacterium tuberculosis (Mtb) is a highly infectious aerosolizable bacterium, which causes upward of 1.5 million deaths per year. Alveolar macrophages, the primary defense cell of the lung, are the preferred host cell of this intracellular bacterium. Vitamin D3 is a known transcription factor, modulating the transcription of pro- and anti-inflammatory cytokines and immunologically relevant proteins. In a vitamin D3 deficient host, the immune systems response to infection is greatly impaired. We used a quantitative systems biology approach to model the impact of long-term vitamin D3 deficiency on macrophage effector response. We then compared our simulation output to our in vitro model of mycobacterium infection of macrophages from vitamin D3 supplemented hosts. Our in silico model results agreed with in vitro levels of hydrogen peroxide (H2O2) production, an antimicrobial effector molecule produced by the host's macrophage, known to be modulated indirectly by vitamin D3. The current model will provide a foundation for further studies into the effects of micronutrient deficiency on immune response.
AB - Mycobacterium tuberculosis (Mtb) is a highly infectious aerosolizable bacterium, which causes upward of 1.5 million deaths per year. Alveolar macrophages, the primary defense cell of the lung, are the preferred host cell of this intracellular bacterium. Vitamin D3 is a known transcription factor, modulating the transcription of pro- and anti-inflammatory cytokines and immunologically relevant proteins. In a vitamin D3 deficient host, the immune systems response to infection is greatly impaired. We used a quantitative systems biology approach to model the impact of long-term vitamin D3 deficiency on macrophage effector response. We then compared our simulation output to our in vitro model of mycobacterium infection of macrophages from vitamin D3 supplemented hosts. Our in silico model results agreed with in vitro levels of hydrogen peroxide (H2O2) production, an antimicrobial effector molecule produced by the host's macrophage, known to be modulated indirectly by vitamin D3. The current model will provide a foundation for further studies into the effects of micronutrient deficiency on immune response.
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U2 - 10.1109/EMBC.2018.8512889
DO - 10.1109/EMBC.2018.8512889
M3 - Conference contribution
C2 - 30440886
AN - SCOPUS:85056615759
T3 - Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBS
SP - 2382
EP - 2385
BT - 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBC 2018
PB - Institute of Electrical and Electronics Engineers Inc.
T2 - 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, EMBC 2018
Y2 - 18 July 2018 through 21 July 2018
ER -