Th161 - Neutrophil Transcriptomic Profile During Streptococcus Pneumonia Infection in Mice

Hernan Peñaloza – Pontificia Universidad Católica de Chile; Omar Vallejos – Pontificia Universidad Católica de Chile; José Cordero – Pontificia Universidad Católica de Chile; Nelson Barrera – Pontificia Universida Católica de Chile; Susan bueno – Full professor, Pontificia Universidad Catóñica de Chile

Abstract Text: Streptococcus pneumoniae (S. pneumoniae) is a Gram-positive bacterium and the main cause of bacterial pneumonia worldwide. When S. pneumoniae colonizes the lower respiratory tract, it is recognized by cells from the host triggering the immune response. In the early stage of lungs infection, neutrophils have a crucial role in bacterial clearance through the release of proinflammatory cytokines, phagocytosis, and neutrophil extracellular traps (NETs) release. However, studies have reported that neutrophils can exert immunomodulatory activity and modulate the inflammation in the lungs. Previous reports of FSClow and FSChigh neutrophil subpopulations present in infected mice showed that the ratio between these 2 subsets change with course of infection but is unknown if this change is related to the presence of a key unidentified component.

Therefore, the study aim was to evaluate the transcriptomic profile of purified neutrophils during S. pneumoniae infection in mice to determine a key factor that could modulate the ratio of the described neutrophil subpopulations. For this, C57BL/6 mice were intratraqueally inoculated with 3x10⌃7 colony forming units, then, 12 and 24 hours post infection, neutrophils were purified from broncho alveolar fluid and RNA-seq was performed. Results showed 4000 differentially expressed genes and gene set enrichment showed cellular pathways related to hypoxia response, damage response, neutrophil response, response cancer, neuroinflammation response, among others. In conclusion, these results shows that neutrophils participate are multifaced cells that help in microbe elimination but also in other unexpected pathways.

Funding: FONDECYT 1231905 & 1211060 and Millennium Institute on Immunology and Immunotherapy ICN09_016 (former P09/016-F).