Viral infection of macrophages reduces CD36 expression: Implications for phagocytosis of non-typeablehaemophilus influenzae

Respiratory viral infections can cause exacerbations of COPD and lead to secondary infections with bacteria such as non-typeable Haemophilus influenzae (NTHi). Previous work has suggested a role for the scavenger receptor B, CD36, in the phagocytic defect induced by influenza infection 1 . The aim of the present study was to investigate how human macrophages regulate their CD36 expression in response to viral infection. Human monocyte-derived macrophages (MDM) were exposed to H3N2 X31 influenza virus or M37 RSV or UV-irradiated virus (UVX31 or UVRSV). No infection of MDM was seen upon exposure to UV-irradiated virus but incubation with X31 or M37 resulted in significant levels of viral detection by flow cytometry (30% nucleoprotein 1+) or RT-PCR (18-fold increase RSV N gene) respectively. Infection significantly decreased cell surface expression of CD36 by MDM at both the cell surface (n=6, 3288 specific mean fluorescence intensity (SMFI) vs 2635 SMFI p=0.047) and mRNA level (p=0.02). This decrease in CD36 expression was reversed by inhibiting influenza infection with Concanamycin A but not in the presence of oseltamivir. Influenza infection did not affect the uptake of fluorescently-labelled latex beads by MDM, but caused a 50% reduction in the phagocytosis of NTHi (p=0.03). Our study identifies a key mechanism by which acute viral infection of macrophages impacts on their phagocytic ability. Further understanding of this pathway may lead to new treatments to reduce the impact of secondary bacterial infection in diseases such as COPD. 1. Wang et al (2012) PLoS ONE.