Manchester-Researchers have found that chewing food prompts the release of an immune cell that can protect against infection.

According to the study team, led by Dr Joanne Konkel of the University of Manchester in the United Kingdom, in the gut and the skin, Th17 cells are produced through the presence of friendly bacteria. However, the researchers note that the mechanisms by which Th17 cells are produced in the mouth have been unclear.

Dr Konkel and colleagues note that the mechanical force required by mastication leads to physiological abrasion and damage in the mouth.  With this in mind, the team set out to investigate whether such damage might play a role in oral Th17 cell production. The researchers came to their findings by feeding weaning mice soft-textured foods, which required less chewing, until they reached 24 weeks of age. At 24 weeks, the release of Th17 cells in the rodents’ mouths was measured.  A significant reduction in oral Th17 cell production was noted, which the team speculated was down to a reduction in mastication-induced physiological damage.

Confirming their theory, the researchers found that increasing the levels of physiological damage in the rodents’ mouths - by rubbing the oral cavity with a sterile cotton applicator - led to an increase in the production of Th17 cells.

Dr Konkel and colleagues believe these findings indicate that chewing food may help to protect us from illness.

Dr Joanne Konkel said, “The immune system performs a remarkable balancing act at barrier sites such as the skin, mouth and gut by fighting off harmful pathogens while tolerating the presence of normal friendly bacteria.

Our research shows that, unlike at other barriers, the mouth has a different way of stimulating Th17 cells: not by bacteria but by mastication. Therefore mastication can induce a protective immune response in our gums.”

In their study, the team also found that long-term exposure to physiological damage caused by mastication can exacerbate the effects of periodontitis.

They came to this finding by feeding weaning mice hardened food pellets up until 24 weeks of age.

Compared with mice fed soft food, the mice fed hard food showed more mastication-induced physiological damage in their mouths and increased periodontal bone loss.

Still, the researchers believe that their findings could lead to new strategies to combat an array of illnesses.

“Importantly, because inflammation in the mouth is linked to development of diseases all around the body,” says Dr Konkel, “understanding the tissue-specific factors that regulate immunity at the oral barrier could eventually lead to new ways to treat multiple inflammatory conditions.” Meanwhile another study suggests that chronic kidney disease affects millions of people in the United States each year. New research points to a circulating protein that may be responsible for the decline in kidney function.


The gene that was named after her may also hold the key to age and life expansion. The Klotho gene was initially identified as a potential age-suppressing gene in mice that could extend the lifespan when over expressed.

There are two types of the Klotho protein - a membrane-bound Klotho and a secreted “soluble Klotho,” which circulates through the blood.

The gene has been shown to regulate some metabolic processes via endocrine pathways, and some studies have uncovered a link between mineral metabolism and aging.

A team of researchers, led by Dr David Drew from Tufts University Medical Centre, set out to examine the link between levels of soluble Klotho and kidney function.

Dr Drew and team were motivated by the insufficient research available on the association between levels of soluble Klotho and changes in kidney function.

Researchers performed a soluble alpha-Klotho assay in 2,496 participants, who were 75 years old on average, from the Health, Aging, and Body Composition study.

The scientists evaluated the link between soluble Klotho and kidney function decline, as well as the incidence of CKD over a 10-year follow-up period.

Findings were adjusted for demographics, comorbidities, estimated glomerular filtration rate, kidney disease risk factors, and mineral metabolism.

Specifically, for each two-fold higher level of soluble Klotho, the scientists found a 20 percent lower risk of kidney function decline at follow-up. These results remained unchanged after adjustment for all the variables, including demographics, CKD risk factors, and mineral metabolism.

The findings seem to suggest, the authors note, that CKD is a condition of soluble Klotho deficiency.

However, the authors advise that future studies should seek to replicate their findings in other populations, and try to uncover the underlying mechanism.

Dr David Drew said that “We found a strong association between low soluble Klotho and decline in kidney function, independent of many known risk factors for kidney function decline. This suggests that Klotho could play a role in the development of chronic kidney disease, although additional research will need to confirm this. This also raises the possibility that Klotho could be an important therapeutic target for future clinical trials.”