SAT0079 The analysis of fecal microbiota in rheumatoid arthritis patients compared to healthy volunteers using bacterial RRNA-targeted reverse transcription-quantitative PCR
Authors: Y. Maeda, M. Matsushita, M. Katayama, M. Yoshimura, A. Watanabe, E. Tanaka, S. Tsuji, A. Kitatobe, Y. Harada, S. Ohshima, Y. Katada, J. Hashimoto, Y. Saeki, T. Takahashi, H. Tsuji, K. Nomoto, K. Takeda
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Gut microbiota have long been thought to contribute to inflammatory disease, and some have considered the bacterial flora as one of the environmental factors causing rhumatoid arthritis (RA). Recently, two gnotobiotic experiments have shown that only one indigenous microflora is critical for the development of arthritis.Wu, et al. have demonstrated that Segmented Filamentous Bacteria induce the differentiation of Th17 cells and cause arthritis in K/BxN mice. Furthermore, Abdollahi-Roodsaz et al. showed the induction of arthritis in IL-1 receptor antagonist-knockout mice by oral administration of <i>Lactobacillus</i> sp. under germ-free condition. In humans, gut microbiota might regulate the host immune systems. Some changes of bacterial flora may cause autoimmune arthritis.On the other hand, new culture-independent genomic analysis techniques of the human microbiome have advanced and make us possible to clarify and quantify in-cultured commensal bacteria. <h3>Objectives</h3> To explore the differences of fecal microbiota between RA patients and healthy volunteers, employing the newly developed the Yakult Intestinal Flora-SCAN (YIF-SCAN®), based on reverse transcription–quantitative PCR (RT-qPCR) using specific primers that target bacterial rRNA molecules. <h3>Methods</h3> Fecal samples were collected from 37 RA patients and 59 healthy volunteers in NHO Osaka Minami Medical Center between January and November, 2011. YIF-SCAN® was performed to quantify the bacterial count with 16S or 23S rRNA-targeted group-specific primers. <h3>Results</h3> Clinical characteristics of both groups are shown in Table 1. There were no statistically significant difference in the bacterial counts and the prevalence of obligate anaerobic bactrerial groups (<i>Clostridium coccoides</i> group, <i>C. leptum</i> subgroup, <i>Bacteroides fragilis</i> group, <i>Bifidobacterium</i>, <i>Atopobium</i> cluster, <i>Prevotella</i>) and <i>C. difficile, C. perfringens</i> between RA and healthy volunteers. Interestingly, Table 2 showed that in facultative anaerobic groups, total bacterial population levels of <i>Lactobacillus</i> (especially <i>L. gasseri, L. reuteri, L. plantarum, L. fermentum subgroup</i>) and <i>Enterococcus</i> were significantly higher in RA. The prevalence of <i>L. reuteri, L. ruminis, L. fermentum</i> subgroup was significantly higher in RA. <h3>Conclusions</h3> We obviously found the differences of fecal microbiota between RA patients and healthy volunteers. Clinical significance of these observations is still unknown.For further understanding of these results, samples of RA patients who have been treated with biologics for 6 months and attained clinical remission are being re-examined for analysis. <h3>References</h3> H-J Wu et al., Immunity 32: 815-827, (2010) S. Abdollahi-Roodsaz et al., J Clin Invest 118: 205-216, (2008) J. U. Scher et al., Nat. Rev. Rheumatol. 7: 569-578, (2011) <h3>Disclosure of Interest</h3> None Declared