Full-length 16S rDNA sequencing based on Oxford Nanopore Technologies revealed the association between gut-pharyngeal microbiota and tuberculosis in cynomolgus macaquesOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreWhat was studied?
This study examined whether the gut and pharyngeal microbiome is associated with tuberculosis (TB) disease stages. Researchers used full-length 16S rDNA amplicon sequencing performed with Oxford Nanopore Technologies to profile bacterial communities. The comparison spanned TB-negative controls, latent TB, and active TB groups. The goal was to identify microbial differences that track with TB progression from latent to active disease.
Who was studied?
The subjects were 71 cynomolgus macaques, an animal model used to study TB pathogenesis. The macaques were divided into three groups: TB (-) control, TB (+) latent, and TB (+) active. No human cohort was involved, so findings reflect a non-human primate model rather than a human population.
What were the most important findings?
In the pharyngeal microbiome, Haemophilus hemolyticus was decreased and Prevotella species were increased in TB (+) macaques compared to controls. In the gut microbiome, Eubacterium coprostanoligenes was enriched in TB (+) macaques. These shifts distinguished infected animals from TB-negative controls, suggesting that specific taxa track with TB status in both the pharynx and the gut.
What are the greatest implications of this study?
The findings suggest that alterations in gut and pharyngeal bacteria may influence host immune regulation and TB severity, though the underlying mechanisms still need to be explored and validated. This work points to potential host-microbe interactions relevant to TB progression that could inform future understanding of disease biology. It also raises the possibility that microbiome-based markers or targets could eventually contribute to TB therapeutics, pending further mechanistic and translational research.