Introduction: 

The colon, as the rest of the GI tract, is covered with a firmly adherent mucus layer which serves as a physical barrier. The mucus layer is important in the colon for preventing colonic bacteria from invading the colonic mucosa and cause inflammation. The regulation of the mucus secretion is poorly understood. In this study, we wanted to investigate if the mucus secretion might be regulated by luminal bacterial products.

Methods: 

Germ Free NMRI mice and conventional NMRI mice were used. The descending colon of anaesthetized (Isoflurane ®) mice was exteriorized and the mucosal surface visualized. The firmly adherent mucus thickness was measured with micropipettes after which the loosely adherent layer was removed by suction. The accumulation of the mucus was measured for 45 min, and the firmly adherent mucus layer was then measured again. In another set of animals PGN or LPS was applied luminally during the 45 min period.

Results: 

The Germ Free animals had hardly any firmly adherent mucus in the descending colon (80 mm), while the convention animals had a 341 mm thick adherent mucus layer. When the colonic mucosa of the germ free animals was exposed to LPS or PGN luminally, the thickness of the adherent mucus layer increased to 293 mm and 351 mm respectively. This effect could not be observed in the conventional animals, which when treated with LPS had an adherent mucus layer as same as in the control situation (332 mm).

Conclusion: 

When treating the germ free mice with LPS and PGN luminally, the firmly adherent mucus layer increases to the levels that we normally can observe in the conventional mice. Since LPS is a TLR2 ligand and PGN is a TLR4 ligand, the mucus secretion could be regulated by bacterial endotoxins or plasma membrane via the TLR2 and TLR4 receptor pathways.