Autophagy is suppressed in peripheral blood mononuclear cells during chronic obstructive pulmonary disease

Abstract

Assessing autophagy promises to provide valuable information regarding the pathogenesis of chronic obstructive pulmonary disease (COPD). However, measuring the dynamic aspect of autophagy is challenging, and sample manipulation can cause signal fluctuations that deviate from the situation in vivo. Our aim was to assess an organotypic method to quantify autophagy in the context of COPD, where autophagy has demonstrated disease-related modulation. Blood from control and COPD participants was treated with/out chloroquine. Protein from peripheral blood mononuclear cells (PBMC) was then isolated and compared for LC3B-II abundance. Our observations show that while basal level LC3B-II abundance was similar between each group (P = 0.60), autophagic flux was significantly lower in the COPD cohort, suggesting disruption in autophagy (P = 0.004). We aim to extend this inquiry and compare pulmonary vs blood samples, to identify the utility of measuring autophagy in blood as a diagnostic outcome predictive of early COPD.