Abstract
Very little is known about disease transmission via the gut microbiome. We hypothesized that certain inflammatory features could be transmitted via the gut microbiome and tested this hypothesis using an animal model of inflammatory diseases. Twelve-week-old healthy C57 Bl/6 and Germ-Free (GF) female and male mice were fecal matter transplanted (FMT) under anaerobic conditions with TNFΔARE−/+ donors exhibiting spontaneous Rheumatoid Arthritis (RA) and Inflammatory Bowel Disease (IBD) or with conventional healthy mice control donors. The gut microbiome analysis was performed using 16S rRNA sequencing amplification and bioinformatics analysis with the HIVE bioinformatics platform. Histology, immunohistochemistry, ELISA Multiplex analysis, and flow cytometry were conducted to confirm the inflammatory transmission status. We observed RA and IBD features transmitted in the GF mice cohort, with gut tissue disruption, cartilage alteration, elevated inflammatory mediators in the tissues, activation of CD4/CD8+ T cells, and colonization and transmission of the gut microbiome similar to the donors’ profile. We did not observe a change or transmission when conventional healthy mice were FMT with TNFΔARE−/+ donors, suggesting that a healthy microbiome might withstand an unhealthy transplant. These findings show the potential involvement of the gut microbiome in inflammatory diseases. We identified a cluster of bacteria playing a role in this mechanism.
Highlights
As research on the immune system has expanded over the last decade, the gut microbiome has been increasingly identified as a key player
After observation of the dysbiosis in TNFΔARE+/−donors and GF fecal matter transplanted (FMT) mice transplanted with sick donors, we looked deeper into the emergent Phyla, performing basic local alignment search tool (BLAST)
We found the same emergent key players already identified in our previous publication linked with TNF mechanisms and functions [1], that have been identified by others in an inflammatory context [10]: Lactobacillus, Escherichia, Bacteroides and Parabacteroides, Actetanaerobacterium, Helicobacter, Clostridium and Lachnoclostridium, Eubacterium, Roseburia, Prevotella and Oscillospira are the microorganisms with the major amplitude changes observed in BLAST TaxID (Figure 6, panel (c))
Summary
As research on the immune system has expanded over the last decade, the gut microbiome has been increasingly identified as a key player. The mechanisms involved in its homeostasis or imbalance and its impact on diseases, treatments, and interactions with the mucosal immune system are described today more and more [1,2,3]. A consensus of bacteria and viruses interacting together is becoming a more. We are still in the observational portion of this discovery, more research is emerging that reveals the specific mechanisms underlying the link between bacteria, their metabolites, and the immune system [2,3] The gut microbiome, comprised of 95% bacteria, fungi, viruses and other microorganisms, is in physiological homeostasis in healthy humans [4,5]. An imbalance, called dysbiosis, results in pathophysiological mechanisms and events leading to metabolic changes and the initiation of disease states [6]
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