Periodontitis exacerbated colitis in mice

Periodontitis can lead to severe inflammation of the intestines — but only in the case that the microbiome latter is already broken. This is the conclusion reached by the team of researchers that has conducted a series of experiments on mice. Scientists have discovered that the basis of this mechanism is the migration of pathogenic bacteria from the oral cavity to the intestines and triggered by their immune response. Detailed results of the study published in the journal Cell.

In recent years, an increasing number of studies on the impact of symbiotic gut microbiome of physical and mental health. However, microorganisms inhabit and other parts of the human body, including the mouth, unfortunately, not all of them are harmless some of them can cause or aggravate serious health problems — for example, periodontitis.

Periodontitis unpleasant by itself, however, there is evidencethat this disease provokes a chronic intestinal inflammation and even colorectal cancer. Scientists assume that this relationship has a bacterial nature, however, clear evidence of this hypothesis yet no one has provided.

A team of researchers led by Nobuchika by Kamada (Kamada Nobuhiko) from the University of Michigan decided to look into this issue in more detail. To do this, scientists conducted an experiment with mice, which overlay alloys called periodontitis. Two weeks later part of the experimental animals were treated with dextran sulfate sodium, to stimulate the development of colitis. As a result, their condition is much deteriorated in comparison with the control group.

In mice suffering from periodontitis, has changed the species composition of bacteria of the oral cavity. Compared to healthy individuals, it increased the share of the family Enterobacteriaceae Enterobacteriaceae, especially species of the genera Klebsiella and Enterobacter. Interestingly, similar changes have occurred in the intestine but only in individuals who, in addition to periodontitis suffered and colitis.

To test whether the bacteria of the oral cavity migrate into the intestine and aggravate his inflammation, the researchers put more experience. Deprived of the microbiome mice were divided into two groups, and then first settled bacteria from healthy individuals and from those suffering from periodontitis. As a result, rodents from the second group developed inflammation of the colon. The same effect of artificially assembled communities of bacteria that mimic the microbiome mice with periodontitis. Scientists have been able to remove inflammation of intestine drug anakinra: it confirmed their hunch that in the process were involved in protein interleukin 1, beta, produced by macrophages.

Bacteria the oral cavity affect the immune system and on a different level. As shown by analysis of mice with periodontitis and colitis, the concentration of T helper 17 in the mucosa of the colon was higher than in individuals with only colitis (p < 0.01). The authors demonstrated that these immune cells first accumulate in the oral cavity, and then migrate to the intestine. Met with bacteria, which came here from the mouth, they activate and amplify the inflammation.

The researchers note that periodontal disease could cause inflammation of the intestine in individuals with a healthy microbiome, is able to repel the colonizers of the oral cavity. Problems arose only in those cases when the intestinal symbionts were oppressed, and surrounding tissues inflamed for other reasons.

Although the study conducted on mice, it cannot automatically be transferred to people, the authors still recommend to carefully take care of your mouth: according to them, it can reduce the risk of problems with the intestines.

According to a recent study, Smoking electronic cigarettes can trigger the growth of biofilms in the oral cavity. It’s all about the influence of glycerol and propylene glycol, which cause changes of the subgingival microbiome to determine the inflammatory process

Sergey Knee High

Leave a Reply

Your email address will not be published.