Frontiers in Immunology

Gum disease may prime immune-cell aging in mice

After 14 days of induced gum disease in male mice, spleen immune cells showed more aging-related changes than controls after laboratory stimulation.

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Mechanisms
Studied:
Experiments in male BALB/c mice, 14 days, against control mice without molar thread
What changed:
After laboratory stimulation, helper T cells from mice with gum disease more often carried aging-related proteins than control cells
The catch:
The increased share of senescence-marker-positive cells appeared only after laboratory stimulation

Editor of record: Boris Djordjevic · AgingResearch.News

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An experiment in male BALB/c mice aged 5–42 weeks tested whether gum inflammation could prime helper T cells, which help coordinate immunity, for senescence, a state in which cells stop dividing. Researchers tied silk thread around upper molars for 14 days and compared the mice with controls without thread.

Before laboratory stimulation, spleen helper T cells showed no significant difference in the share carrying two senescence-associated proteins. After stimulation for up to three days, spleen-cell cultures from mice with gum disease showed more signs of senescence and released more inflammatory substances. The share carrying both proteins peaked in cells from 18-week-old mice. Transferring stimulated helper T cells from mice with gum disease into mice lacking functional T cells worsened experimentally induced arthritis compared with cells from controls.

Why it matters

Age-related immune changes contribute to rheumatoid arthritis. The findings bear on whether inflammation around teeth can shape immune-cell changes involved in disease elsewhere in the body.

Caveats

The increased share of cells carrying both senescence-associated proteins appeared after laboratory stimulation. These male-mouse and cell-transfer experiments do not establish that the same process occurs in people.

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