Excess inflammation impaired colon repair in old mice
Experiments monitored mice aged 2–3 and 20–22 months for three weeks after bacterial infection; older animals showed poorer repair of the colon lining.
Limit: Inflammatory sensitivity experiments used small-intestine organoids rather than living colons
Stake: An author works for Genentech. An author holds shares in Roche.
Edited by Boris Djordjevic · AgingResearch.News
In experiments in mice aged 2–3 months and 20–22 months, researchers infected the animals with the gut bacterium Citrobacter rodentium. After infection, a disproportionate inflammatory response in old mice accompanied impaired repair of the colon lining. Ten days after infection, about 95% of crypts, small pockets in the lining, were damaged in the examined end section of old colons, compared with about 60% in young colons.
Immune cells in old colons produced more interferon gamma, an immune signaling protein. This was associated with reduced numbers of one type of intestinal stem cell and less cell division. Old intestinal lining cells showed elevated activity of genes normally active during fetal development. In colon organoids, miniature tissue models grown in the lab, those from old mice were more sensitive to interferon gamma-induced cell death than those from young mice.
Why it matters
Many tissues lose regenerative capacity with age. This work addresses how interactions between inflammation and stem cell function may contribute to that decline.
Caveats
The repair findings came from bacterial infection experiments in mice, not people. Experiments testing the sensitivity of fetal-like cell states used small-intestine organoids rather than living colons.
