Otitis-prone children are characterized by differential expression of selected genes in peripheral blood mononuclear cells (PBMC) during their healthy stages and during acute otitis media (AOM) episodes, according to data presented at the ASM Microbe 2016 meeting.
Ravinder Kaur, PhD, of Rochester General Hospital, and colleagues studied the blood samples of children who experience recurrent ear infections, called otitis-prone, compared with children who have few ear infections. They examined the blood samples during their AOM state and during a healthy state.
The researchers extracted and sequenced RNA from PBMC of 12 children between 9 and 12 months. They conducted a differential expression analysis to compare otitis-prone patients with non-otitis-prone patients. A total of 13 528 genes were analyzed for differential expression in healthy visits and 13 248 genes were analyzed in AOM visits.
Dr Kaur and colleagues noted significant expression differences in 39 genes during a healthy state, and in 31 genes during an AOM state in otitis-prone children (P<.0003; q≤.1).
In a healthy state, the complement and coagulation cascades pathway was differentially downregulated in otitis-prone children in genes C1, C2, C1qA, and C3AR1 (P=.0006). The pathway was a mediator for innate immunity that lead to the direct killing of pathogens and the recruitment of inflammatory and immunocompetent cells, which suggests that otitis-prone children have a weak innate immunity to defend the pathogens, the researchers explained.
During the infection state in otitis-prone children, the researchers noted an upregulation of genes that was shown to regulate the functions of chemical signaling pathways, cell differentiation, and apoptosis that indicates more cell death and damage to the host during infection.
Kaur R, Kennedy R, Casey J, et al. Abstract 604. Differential characterization of gene expression patterns in PBMC of children who have recurrent middle ear infections compared to non-otitis prone. Presented at the American Society for Microbiology Microbe 2016; June 16-20, 2016; Boston, MA.