Chronic alcohol abuse has been shown to alter immune defense mechanisms in humans and mice which makes the host susceptible to infections, including Mycobacterium tuberculosis (Mtb) infection. However, limited information is available on the mechanisms involved in alcohol-mediated host immune system dysfunction.
In this study, we determined the effects of ethyl-β-d-glucuronide (EtG), an alcohol-derived metabolite, on immune response of mice lung macrophages. We measured cytokine and chemokine production by gamma-irradiated mtb (γ-mtb) stimulated mice lung macrophages in the presence or absence of EtG. We also determined the effect of EtG on the metabolic state of γ-mtb stimulated mice lung macrophages.
We found that EtG inhibited secretion of IL-10 and enhanced production of macrophage inhibitory protein (MIP-1ß). We also found that EtG significantly inhibits oxidative phosphorylation of lung macrophages stimulated with γ-mtb.
Date of publication
Ramakrishna Vankayalapati, PhD (Thesis Director), Mitsuo Ikebe, PhD, Torry Tucker, PhD, Samten Buka, MD.
Master of Science in Biotechnology
Inaku, Charles, "FUNCTIONAL IMPACT OF ETHYL-β-D-GLUCURONIDE ON MYCOBACTERIUM TUBERCULOSIS STIMULATED LUNG MACROPHAGES" (2023). Biotechnology Theses. Paper 7.