Influenza A Virus Impairs Neutrophil Antibacterial Responses Against Streptococcus pneumoniae

Authors: Chloe Picciano, Elsa Bou Ghanem, Alexsandra Lenhard, Bruce Davidson

SUNY Campus: SUNY Buffalo

Presentation Type: Poster

Location: Old Union Hall

Presentation #: 45

Timeslot: Session C 1:45-2:45 PM

Abstract: Streptococcus pneumoniae (pneumococcus) are Gram-positive bacteria that asymptomatically colonize the nasopharynx. Influenza A Virus (IAV) infection is a major risk factor for the transition of pneumococci from asymptomatic colonizers to disease-causing pathogens. Neutrophils, or PMNs, are innate immune cells that function to kill and clear bacteria in several different ways. IAV infection significantly impairs the ability of PMNs to kill pneumococci. This study aimed to determine which PMN antimicrobial effector function(s) are impaired upon IAV infection. We utilized a novel murine model to study the effect of IAV/S. pneumoniae co-infection on PMN responses. All experiments used PMNs isolated from the bone marrow of IAV- and mock-infected mice two days post infection. We used a flow cytometry-based assay and found no difference in percent of intracellular and extracellular bacteria between IAV-infected and naïve hosts, suggesting that phagocytosis is not impaired. Next, to determine if the production of intra- vs. extracellular reactive oxygen species (ROS) is altered, we ran a plate-based chemiluminescent assay. We found intracellular ROS production was significantly increased in PMNs isolated from IAV-infected hosts. To examine this further, we are performing assays to determine which source of intracellular ROS is dysregulated in this model, and if increased or decreased production from either of the sources impairs bacterial killing by PMNs. Advancements in our understanding of PMN function in IAV/S.pneumoniae coinfection can help improve therapies to boost host defense in coinfection.