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New Research Examines Factors That Control Oral Immune Responses

New Research Examines Factors That Control Oral Immune Responses According to a study published online in Immunity, barrier sites in the body—including the skin, oral cavity, and intestines—routinely host harmful substances and infectious microorganisms. Of course, these sites also contain

New Research Examines Factors That Control Oral Immune Responses

According to a study published online in Immunity, barrier sites in the body—including the skin, oral cavity, and intestines—routinely host harmful substances and infectious microorganisms. Of course, these sites also contain harmless microbes. The immune system must differentiate between the two, and new research focusing on Th17 immune cells reveals how microorganisms and the immune system work together to preserve oral health.

As reported in “Ongoing Mechanical Damage From Mastication Drives Homeostatic Th17 Responses at the Oral Barrier,” researchers found that subjects with genetic defects in Th17 cell function are more susceptible to oral infections than those with normal cell function. Building their research on evidence of the interaction of microorganisms and the immune system, the researchers observed that Th17 immune cells increase with age. This led to the hypothesis that this is due to an increase in oral microbes. A closer look at the oral microbial load in a mouse model, however, revealed that mice at 8 weeks and 24 weeks presented with comparable bacterial levels. The team also compared the bacterial levels of mice raised in a clean environment with those raised in a nonsterile environment. Again, the microbial load was consistent between the two groups. This led to the conclusion that factors regulating these cells are dependent on unique site characteristics.

Using this information, the team focused on the signaling molecule IL-6, which is necessary for Th17 immune cell accumulation. After examining factors that promote IL-6 and Th17 accumulation at the oral barrier, they theorized that chewing triggers an immune response—which was confirmed by observing mice raised on a soft-food diet (ie, minimal chewing) vs those fed a normal diet (average chewing). The results show that Th17 levels rose in mice fed a normal diet, but did not affect mice lacking IL-6. The investigators concluded that mechanical forces trigger Th17 cells as a protective immune response. Overstimulation of these cells may contribute to inflammation and periodontal diseases, however, making regulation essential to oral health.

Hygiene Connection E-Newsletter

February 2017

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