GSE137351
Global changes in human neutrophil transcriptome profile during Filifactor alocis challenge
Periodontitis is a multifactorial chronic inflammatory infectious disease with a high prevalence in the adult population in the USA. Until recently, research into periodontitis focused primarily on putative pathogens such as Porphyromonas gingivalis. However, a reappraisal of microbial etiology has marked a turning point in the field due to the development of culture-independent techniques that allow the identification of bacterial species directly from nucleic acids. Filifactor alocis, a Gram positive anaerobic oral bacterium, has emerged as an important periodontal pathogen. Neutrophils are recruited in high numbers to the gingival tissue, where they are linked with protection against periodontal disease. However, periodontal pathogens evolved different strategies to resist neutrophil microbicidal mechanisms while propagating inflammation, which affords a source of nutrients. The goal of this study was to determine the global changes in human neutrophil gene expression induced by F. alocis challenge.  RNA-sequencing analysis shows that F. alocis-challenge alters human neutrophil transcriptome including expression of genes associated with regulation of Toll-Like Receptor signaling pathway, MAPK signaling pathway, apoptosis, cytokines and chemokines, among other neutrophil effector functions. Overall design: A total of 16 samples were submitted for RNA-sequencing analysis. Those 16 samples corresponded to four independent donors, with four experimental conditions, as outlined on the treatment protocol section, per donor. Unstimulated neutrophils were used as negative controls.