## 7 The Oral Microbiota and Gut Microbiota Axis  
Literature linking the microbiota of the human oral to the gut microbiota is gaining momentum, and the \"oral-gut axis\" has been recently proposed [49]. In the study by [PERSON] et al., a group of gastroenterologists, dentists, and researchers studied the role of the intramucosal connections between the gut and oral cavity of patients with IBD. SPF mice mimicking a periodontitis phenotype (SPF-ligature) and normal healthy controls (HC) were treated with dextran sodium sulfate (DSS) to induce colitis. Before treatment with DSS, SPF-ligature mice showed oral dysbiosis compared to controlsas well as promotion of a Th1 response into the lamina propria via increased immune infiltration of Th17 cells, B cells, and T cells. After DSS treatment, greater inflammation in the colonic mucosa showed increased myeloid and lymphoid infiltration and further isolation of CD3\({}^{+}\)CD4\({}^{+}\) T cells from SPF-ligature DSS mice as well as higher production of IL-17A and interferon gamma (IFN-\(\gamma\)) compared to control mice [49]. The oral and gut microbiota of SPF-ligature DSS mice showed that specific oral-originating bacteria were found to colonize both environments. Using linear discriminant analysis effect size (LEfSe), _Klebsiella_ spp. and _Enterobacter_ spp. from the bacterial family Enterobacteriaceae, were predominately found in the oral cavity of disease models as well as in accumulation in the gut and were not found in non-ligature DSS controls [49]. In general, Enterobacteriaceae is the most predominant bacterial taxon found in the oral cavity during periodontitis infections, and these results indicate that non-periodontitis DSS mice were protected from ectopic colonization of oral-derived pathobionts while the periodontitis-DSS mice were greatly susceptible. Increased inflammation and infiltration of gut immune cells initiated by periodontitis ligatures showed that DSS-treated mice were more likely to have oral-derived pathobiont colonization in the gut, thus supporting the \"oral-gut axis\" paradigm. In another study, [PERSON] et al. showed that colitis-induced mouse models have a significant association between saliva microbial profiles and proximal gut profiles reflective to the proportion of inflammation [110]. Additionally, a recent study published by [PERSON] et al., reported evidence supporting the relationship between oral and gut microbiota [111] and a more expanded overview of relative oral-gut bacteria composition is summarized in Table 1. Saliva samples from two patients with IBD were transplanted into C57 BL/6 (B6) GF mice and examined for immunological changes in colonic and small intestinal lamina propria tissue; B6 GF mouse saliva was also examined before and after IBD saliva transplantation. Tissue taken from small intestinal lamina propria showed a significant increase in the relative amount of IFN-\(\gamma\)-producing CD4\({}^{+}\) Th1 helper cells as well as fecal microbiota composed of many oral-originating bacterial species, particularly _Klebsiella pneumoniae_[111]. When administered orally, isolated _K. pneumoniae_ was also found to contribute significantly to the induction of Th1 cells in the oral cavity and colon [111] and significantly attributed to greater expression of colonic lamina propria CD4\({}^{+}\) T cells producing IL-17 (Th17 cells) and IFN-\(\gamma\) in colitis-prone IL-10 knockout mice [111]. These results infer that in susceptible patients, the effect of oral-originating _K. pneumoniae_ pathobiont could contribute to the induction of significant immune responses and IBD pathogenesis. It should also be noted that increased production of IFN-\(\gamma\) by memory CD4\({}^{+}\) T cells in addition to increased production of IL-17-secreting Th17 cells leads to further production of proinflammatory cytokines IL-6, IL-1, and TNF-\(\alpha\) and may be related to the IL-23/Th17 axis as mentioned in earlier sections.