Oral primo-colonizing bacteria modulate inflammation and gene expression in bronchial epithelial cells

The microbiota of the mouth disperses into the lungs and both compartments share similar phyla. Considering the importance of the microbiota in the maturation of the immunity and physiology during the first days of life, we hypothesized that primo-colonizing bacteria of the oral cavity may induce immune responses in bronchial epithelial cells. Herein, we have isolated and characterized 57 strains of the buccal cavity of two human new-borns. These strains belong to Streptococcus, Staphylococcus, Enterococcus, Rothia and Pantoea genera; Streptococcus being the most represented. The strains were co-incubated with a bronchial epithelial cell line (BEAS-2B) and we established their impact on a panel of cytokines/chemokines and global changes in gene expression. The Staphylococcus strains, which appeared soon after birth, induced a high production of IL-8, suggesting they can trigger inflammation, whereas the Streptococcus strains were less associated with inflammation pathways. The genera Streptococcus, Enterococcus and Pantoea induced differential profiles of cytokine/chemokine/growth factor and set of genes associated with maturation of morphology. Altogether, our results demonstrate that the micro-organisms, primo-colonizing the oral cavity, impact immunity and morphology of the lung epithelial cells, with specific effects depending on the phylogeny of the strains. The overall design consisted of 7 samples of BEAS-2B cells treated with Streptococcus EMS321, Streptococcus EMS383, Streptococcus EMS3101, Enterococcus EME126, Enterococcus EME141, Enterococcus EME343 and Enterococcus EME394 versus unchallenged BEAS-2B cells. A minimum of four dye-swap hybridizations (4 biological replicates) were performed for each of the 7 samples analyzed. Unchallenged BEAS-2B cells were controls and challenged BEAS-2B cells with the bacterial strains were treated samples.