Abstract
Crohn’s disease causes chronic inflammation in the gastrointestinal tract and its pathogenesis remains unclear. In the intestine of Crohn’s disease patients, CD14+CD11+CD163low macrophages contribute to inflammation through the induction of Th17 cells and production of inflammatory cytokines; the CD14+CD11c+163high fraction is anti-inflammatory through the production of IL-10 in normal cases. In this report, the 16S rRNA gene amplicon sequencing method was used to identify bacteria that are specifically present in intestinal CD14+CD11c+ macrophages of Crohn’s disease patients. Bacteria present in intestinal CD14+CD11c+ macrophages and mucus of Crohn’s disease patients were separated into different clusters in principal coordinates analysis. There was a statistically significant increase in the relative composition of CD14+CD11c+ macrophages from mucus in two phyla (Proteobacteria [p = 0.01] and Actinobacteria [p = 0.02]) and two families (Moraxellaceae [p < 0.001] and Pseudomonadaceae [p = 0.01]). In addition, OTU-1: Acinetobacter and OTU-8: Pseudomonadaceae tended to concentrate in the CD14+CD11c+CD163low subset, whereas OTU-10: Proteus, OTU-15: Collinsella tended to concentrate more in the CD14+CD11c+CD163high subset than the other subset and mucus.
Highlights
Crohn’s disease causes chronic inflammation in the gastrointestinal tract and its pathogenesis remains unclear
It was suggested that bacteria in macrophages tended to decrease monopolistic operational taxonomic unit (OTU) and increase evenness compared with bacteria in mucus
This study is the first report to comprehensively analyze the bacterial flora in macrophages in the human intestinal lamina propria of Crohn’s disease patients by NGS
Summary
Crohn’s disease causes chronic inflammation in the gastrointestinal tract and its pathogenesis remains unclear. In the intestine of Crohn’s disease patients, CD14+CD11+CD163low macrophages contribute to inflammation through the induction of Th17 cells and production of inflammatory cytokines; the CD14+CD11c+163high fraction is anti-inflammatory through the production of IL-10 in normal cases. The CD14+CD11c+CD163low fraction of normal intestine induces differentiation of Th17 cells; in Crohn’s disease, this induction capability has been accelerated by increased production of inflammatory cytokines[5]. It has been reported that TNF-α production was enhanced in a macrophage cell line infected with Escherichia coli isolated from Crohn’s disease patients[9] These reports suggest that some bacteria from Crohn’s disease patients may survive in the host intestinal macrophages and activate an inflammatory response. There is limited knowledge about the bacterial flora present in macrophages, and in particular regarding the microbiota in macrophages from the intestinal lamina propria of Crohn’s disease patients
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