Villous Movement: Function, Role & Diseases

Villous movements take place within the small intestine. Finger-shaped elevations of the mucosa are located there. These are called villi.

What are villous movements?

Villous movements take place inside the small intestine. Finger-shaped elevations of the mucosa are located there. These are called villi. The mucosa of the small intestine (intestinal mucosa) lines the duodenum, jejunum, and ileum. The intestinal mucosa does not form a smooth surface, but lies in folds. These folds, up to one centimeter high, are also called Kerck ring folds or plicae circulares. They are formed from mucosa and submucosa. The muscle layer of the mucosa is not involved. Another typical feature of the mucosa of the small intestine are the villi intestinales. These are finger-shaped or leaf-shaped protrusions of the mucosa, which are conspicuous as elevations 0.5 to 1.5 millimeters high. At these sites, the mucosa presents with a single-layered, prismatic epithelium. In the center of each villus there is a so-called chyle vessel and a network of many small blood vessels (capillaries). Lymphatic fluid flows through the chyle vessel. In addition, muscle fibers pull into each intestinal villus. This allows the villi to move and deform. Between the villi are the Lieberkühn crypts, which secrete numerous enzymes. The cell pole of the cells sitting on the villi bears microvilli. These small cells are also called brush cells.

Function and task

Kerck ring folds, intestinal villi, and microvilli serve to increase the surface area of the small intestine. With a total length of about three to six meters, the special surface area of the small intestine provides an amazingly large absorption area of 100 to 240 m². That the villi are capable of independent movement could initially only be concluded from the histology of the protrusions. Each villus has fibers of smooth muscle. These fibers traverse the villi longitudinally. From these observations, pathologists in the 19th century concluded that the villi must be able to move. However, direct observation of villi movement was not possible until 1914. This showed that the villi contract individually and do not follow a communal pattern. In a dog, about six contractions per minute per villus were observed in 1927. It is interesting to note that the villi shorten but do not thicken. Instead, the mucosa folds. This change in shape suggests that during these contractions the contents of the villi are squeezed out. The villi serve to absorb nutrients such as sugar, protein or fat components. The squeezing out of the contents of the villi probably takes place into the lymphatic spaces of the submucosa. Depending on the intestinal section, 2000 to 4000 villi per square meter are found in humans. Based on this number, it is possible to calculate the large quantities of nutrients that can be absorbed thanks to the pumping villi movements. The villi movements are controlled by the parasympathetic and also the sympathetic nervous system. Weak stimuli from the vagus nerve stimulate the villi to move; when the vagus nerve is strongly stimulated, the villi become flaccid and stop moving. In addition, the villi are also stimulated by hormones. One hormone that controls villus movement is villikinin.

Diseases and disorders

In many diseases of the intestine, the villi are affected. One disease that damages and destroys many villi is celiac disease. It is an intolerance to gluten. Those affected are hypersensitive to gluten, a gluten protein found in many grains. Food containing gluten causes severe inflammation of the intestinal mucosa in patients. Large areas of the intestinal epithelial cells and thus also the villi are destroyed. Thus, villi movement is no longer possible. Nutrients can only be absorbed very poorly, and most of the food remains undigested in the intestine. This leads to weight loss, vomiting, diarrhea or loss of appetite. Fatigue and depression can also be symptoms of celiac disease. A similar pathophysiology and thus similar symptoms are seen in wheat allergy. In industrialized nations, the disease is estimated to affect around one to two percent of the population. There is no causal treatment. The only option for those affected is a lifelong gluten-free diet. This allows the intestinal mucosa to recover.The villi also rebuild and can move normally. This is important because otherwise permanent deficiency symptoms would result. Damage to the villi and restricted villous motility is also evident with a deficiency of folic acid and vitamin B12. A deficiency of vitamin B12 can have various causes. For example, chronic gastritis (inflammation of the gastric mucosa) can lead to a deficiency of intrinsic factor. Without intrinsic factor, vitamin B12 cannot be absorbed in the intestine. Too little intake or a faulty colonization of the intestine can also trigger a B12 deficiency. Due to a lack of DNA synthesis, a deficiency of folic acid and B12 leads to anemia. Food intolerances are also common. These could be a result of the lack of villous movement. Two diseases associated with villous atrophy and immobility of the intestinal villi are microvillous inclusion disease and tufting enteropathy. Microvillous inclusion disease (MVID) is congenital. Immediately after birth, life-threatening diarrhea occurs due to poor intestinal absorptive capacity. There is a risk of dehydration. Affected children often have to undergo a small bowel transplant shortly after birth. Tufting enteropathy is also congenital. It also manifests as severe diarrhea, and here, too, small bowel transplantation can hardly be avoided.