Title:Complement 3 Receptor Expression in Individuals with Type 2 Diabetes
Volume: 11
Issue: 2
Author(s): Judy Ly, Devin Morris, Minette Lagman, Christopher Ng, Shelby Anderson, John Daliva, Naji Muwanas, Igal Tarash, Cesar Ochoa, Airani Sathananthan and Vishwanath Venketaraman
Affiliation:
Keywords:
Diabetes, tuberculosis, glutathione, complement receptors, immune responses.
Abstract: Background: According to the World Health Organization, as of 2014 9% of the
world’s adult population is affected by diabetes. Uncontrolled diabetes is a pro-inflammatory
process that increases generation of reactive oxygen species (ROS).
Methods: The production of ROS leads to a chronic increase in oxidative stress which results
in an increased susceptibility to infections. Individuals with type 2 diabetes mellitus (T2DM)
are highly susceptible to Mycobacterium tuberculosis (M. tb) infection. Previous research has
demonstrated that glutathione (GSH) plays an important role in the control of M. tb infection.
Recent studies have demonstrated that phagocytosis of M.tb is diminished in patients with
T2DM. Phagocytosis in macrophages is thought to be mediated in part by complement protein
3b (C3b)-complement protein receptor 3b (C3R) interactions. Since C3b production is not diminished
in patients with T2DM we propose that C3R production is reduced and is the cause
for impaired macrophage phagocytosis as well as IL-12 and IFN-γsignaling.
Conclusion: This study utilizes a quantitative PCR (qPCR), demonstrating decreased transcription
of C3R mRNA in patients with T2DM as compared to non-diabetics.
