Two Bacteria that Contribute to Chronic Constipation Identified

Researchers at Nagoya University in Japan have pinpointed two gut bacteria, Akkermansia muciniphila and Bacteroides thetaiotaomicron, that working together contribute to chronic constipation. These microbes destroy the intestinal mucus coating, known as colonic mucin, which normally lubricates the colon, hydrates stool, and protects gut walls from bacterial invasion. When they over-degrade this coating, stool turns dry and stuck, leaving millions with symptoms that resist typical treatments. The study, detailed in Gut Microbes, also reveals why laxatives often miss the mark for those with this persistent issue. 

Constipation ranks as a widespread digestive complaint, commonly blamed on sluggish gut motility where food stalls in the intestines. This view falls short for chronic idiopathic constipation (CIC), which lacks an obvious trigger, and for severe cases in Parkinson's disease patients. Those individuals battle unrelenting constipation 20 to 30 years before tremors appear, a pattern separate from CIC yet equally baffling until now.

The team zeroed in on mucin, the gel-like shield lining the large intestine and mixing into stool. It keeps contents moist for easy transit and bars bacteria from harm. B. thetaiotaomicron starts the attack by using enzymes to strip away sulfate groups that shield mucin. This exposes it for A. muciniphila to break down and consume the exposed mucin. Sulfate barriers usually thwart such degradation; without them, moisture vanishes, stool hardens, and blockages form. Since the core problem lies in mucin erosion rather than slow movement, drugs targeting motility provide little help.

Parkinson's patients carry higher loads of these bacteria, with constipation emerging decades before they develop tremors and movement problems. Past explanations pinned it solely on nerve degradation, but evidence now implicates microbial action in early symptom buildup.

To test this, “We genetically modified B. thetaiotaomicron so it could no longer activate the enzyme sulfatase that removes sulfate groups from mucin,” explained Tomonari Hamaguchi, lead author of the study. “We put these modified bacteria into germ-free mice together with Akkermansia muciniphila, and surprisingly the mice did not develop constipation; the mucin stayed protected and intact.” Blocking sulfatase preserved the layer fully, proving the duo's sequential role.

This breakthrough points to sulfatase inhibitors as potential drugs for bacterial constipation, including in Parkinson's.