Regulatory effects of oral microbe on intestinal microbiota and the illness

Abstract

Over the past decade, the association between oral health, intestinal microbiota, and systemic diseases has been further validated. Some oral microbial species have been isolated from pathological intestine mucosa or feces and identified as biomarkers for intestinal diseases. A small proportion of oral microbiome passes through or colonizes the lower gastrointestinal tract, even in healthy individuals. Opportunistic pathogens from the oral cavity may expand and participate in the occurrence and progression of intestinal diseases when the anatomical barrier is disrupted. These disruptors interact with the intestinal microbiota, disturbing indigenous microorganisms, and mucosal barriers through direct colonization, blood circulation, or derived metabolite pathways. While interacting with the host's immune system, oral-derived pathogens stimulate inflammation responses and guide the transition of the intestinal microenvironment from a healthy state to a pre-disease state. Therefore, the oral-gut microbiome axis sheds light on new clinical therapy options, and gastrointestinal tract ecology balance necessitates simultaneous consideration of both oral and gut microbiomes. This review summarizes possible routes of oral microbes entering the intestine and the effects of certain oral bacteria on intestinal microbiota and the host's immune responses.

Keywords: gut diseases; immunity; intestinal microbe; microbiota; oral microbe; oral-gut axis.

Figure 1

Transient physiological bacteremia triggered by periodontitis and dental procedures permits oral pathogens to stretch themselves systemically. Patients with periodontitis possess a less diverse gut microbiota, and higher possession of oral taxa in the intestine gives rise to more serious gut inflammation (Lourenvarsigmao et al., 2018). To tolerate the inactivation of stomach acid and bile acid, these unexpected “visitors” are expected to be highly acid-resistant. Moreover, P. gingivalis and F. nucleatum can be parasitic on dendritic cells or macrophages and disrupt extraoral tissues (Carrion et al., 2012; Xue et al., 2018). Oral microbes, including P. gingivalis, Actinomyces, Streptococcus, and Treponema denticola, have been confirmed as sources of non-oral organs in a colonizing manner (Figuero et al., 2014; Zhang et al., 2021; Deppe et al., 2022). Chronic oral infection establishes F. nucleatum colonization that significantly induces systemic humoral IgG and IgM antibody responses (Velsko et al., 2015).

Figure 2

To maintain ecological balance, intestinal protective elements resist extra-intestinal microbes in the oral-derived microbiome dysbiosis. In the intestine, the enteral translocation of periodontopathic bacteria brings about gut microbiota dysbiosis and intestinal inflammation, thus weakening the intestinal surface liquids and junctional components (Nakajima et al., 2015; Feng et al., 2020). While interacting with the host’s immune system, via enteral route or hematogenous route, oral-derived pathogens regulate the constitution and transformation of immune cells, guiding the transition of the intestinal microenvironment from a healthy state to a pre-disease state. In regard to cell signaling pathways, cells of Paneth autonomously sense a series of oral metabolites via MyD88-dependent toll-like receptor (TLR), then stimulate antimicrobial cytokines and trigger the downstream NF-kB pathway, which subsequently regulates the production of a series of inflammatory cytokines (Vaishnava et al., 2008; Qi et al., 2022).