leukotriene-c4 and Intestinal-Diseases

Mucosal damage is commonly observed in food-sensitive enteropathy in infants, and the generation of leukotrienes is involved in the pathogenesis of this enteropathy. Because supplementing n-3 fatty acids is known to modify the production of leukotrienes, we investigated whether a change of dietary fatty acid composition affects leukotriene synthesis and food hypersensitivity reactions in the intestine by using a mouse model of food-sensitive enteropathy. The model was prepared by feeding ovalbumin to BALB/c mice after intraperitoneal injection of cyclophosphamide. Diets were prepared from soybean oil (control), perilla oil, lard, corn oil, and 0.125 volume of corn oil (low fat diet) and given to mice for 4 wk. Villous heights, crypt depths, leukotriene B4 and C4 production in the intestine were measured. Crypt hyperplasia and villous atrophy were severer in the corn oil-fed group than those of control group, whereas mucosal damage in the perilla oil and low fat diet groups was minimal. In the corn oil-fed group, red blood cell membrane levels of n-3 fatty acids were lower than the control, and the synthesis of leukotrienes was highest among all groups. In the perilla oil and low fat diet groups, n-6 fatty acids were lower than those of control group and leukotriene production was significantly suppressed. These results indicate that reducing cell membrane levels of n-6 fatty acids by feeding less n-6 fatty acids or supplementing n-3 fatty acids, is important to suppress leukotriene biosynthesis for prevention from mucosal damage in food-sensitive enteropathy.

Topics: Animals; Dietary Fats, Unsaturated; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Female; Food Hypersensitivity; Intestinal Diseases; Intestinal Mucosa; Leukotriene B4; Leukotriene C4; Mice; Mice, Inbred BALB C

The effects of dietary pretreatment on longitudinal ulcers of the intestine induced by indomethacin given intracolonically were investigated in rats. The rats were pretreated with either standard diet or liquid meals. Intracolonic indomethacin (24 mg/kg/day) given for two days produced longitudinal ulcers and small scattered ulcers in the small intestine in the control rats that were receiving standard pelleted formula. Three days pretreatment with one of two types of liquid meals, low residual diet (LRD) or elemental diet (ED), significantly reduced the incidence (3% in ED group and 0% in the LRD group) and the length of the longitudinal ulcers in the small intestine. The caecum was affected in each dietary pretreatment group (67% in controls, 80% in LRD group, and 69% in ED group). Colonic ulcers that were located in a longitudinal fashion were found in 42% of LRD group, while these ulcers were less frequently found in the ED group (13%) and controls (0%). Development of ulcers in the caecum and in the colon of rats in ED and LRD groups was more delayed than that of small intestinal ulcers of control rats. In another experiment, pretreatment by ED significantly increased colonic tissue leukotriene B4 concentration when compared with that of controls. These findings suggest that the site of experimental enteropathy induced by indomethacin given intracolonically can be modified by dietary pretreatment. This animal model can be available for investigating differences in the pathophysiology of enteropathy according to the site of involvement.

Topics: Animals; Diet; Food, Formulated; Indomethacin; Intestinal Diseases; Intestinal Mucosa; Leukotriene B4; Leukotriene C4; Male; Rats; Rats, Wistar; Ulcer