Goblet cell changes during intestinal adaptation to azoxymethane and enteric bypass in the rat

Abstract

Summary Numbers of intestinal goblet cells containing specific acid mucins were determined in male Sprague-Dawley rats receiving azoxymethane (total dose 90mg kg-1) with or without jejunoileal bypass (JIB). Controls During the latent period of experimental colonic carcinogenesis, changes occur in the relative proportions of specific acid mucins elaborated by the goblet (mucous) cells. Twenty weeks after exposure to azoxymethane or dimethylhydrazine, rats show a substantial increase in the number of goblet cells containing sialomucins as opposed to sulphomucins (Filipe, 1975;. A similar and largely specific hyperplasia of sialomucin cells characterises the adaptive response of the colon and functioning jejunoileum to subtotal enteric bypass, as performed for morbid obesity in man (Olubuyide et al., 1984). Since this operation stimulates neoplasia as well as hyperplasia in rat large intestine , the distribution of acid mucins was investigated in animals receiving carcinogen with or without jejunoileal bypass. (n = 17), as previously described Olubuyide et al., 1984). Animals received Oxoid SGI breeding diet (H.C. Styles and Son, Bewdley, Worcs., UK) and water ad libitum. Quarters were lit with alternate 12 h cycles. Besides being weighed weekly, rats were examined daily for evidence of rectal bleeding and diarrhoea. Moribund animals (n = 10) were sacrificed prematurely and autopsied to ascertain the cause of death. Food and water consumption was measured weekly by cage. Materials and methods FortySurviving animals (n = 32) were killed 30 weeks postoperatively by cervical dislocation after exposure to ether. The entire intestinal tract was removed, freed of fat and adhesions and flushed clean with saline. The length of the duodenum (pylorus to ligament of Treitz) and the large intestine (ileocaecal valve to anus) was measured immediately after suspension of the bowel by a fixed weight (3.9 g) against a vertical scale. These segments of gut were laid flat and opened along the antimesenteric border. The mucosa was scrutinised, and all tumours were recorded, excised and fixed in 10% formalin for subsequent histological and histochemical examination, after which the bowel was mopped dry and weighed. Short segments of non-tumour-bearing bowel were cut from the duodenum (mid-way between pylorus and ligament

Neutral and Acidic Goblet Cell Concentrations in the Small Intestine of the Unweaned Pig

“…Brown et al [22] have suggested that these changes may re flect a maturation of the goblet cell as it migrates up the villi. While several studies have found similar staining results [17,19,20], Subbuswamy [16] observed that goblet cells lining the villi in jejunum and ileum stained almost entirely PAS+.…”

“…Differentiated goblet cells migrate with the columnar cells up the villi, releasing a mucous layer over the epithelial surface of the intestinal tract [5][6][7][8]. This mucous layer is important for the pro tection of the underlying mucosa by exclud ing irritants such as antigens, toxins, and gastrointestinal enzymes [9][10][11][12], Other func tions that have been attributed to the mu cous layer are lubrication of the surface for the facilitation of luminal content passage [12,13], removal of parasites [14], and maintenance of a fairly constant pH at the unstirred surface layer [12,15], There have been several histochemical studies of intestinal epithelial mucosubstances in many species under normal con ditions [16][17][18], and in altered states [19,20]. Studies in the pig have been under taken by Rahko and Saloniemi [21] and Brown et al [22], The above studies, of a qualitative nature, have been limited to a few specific areas in the small intestine.…”

Overexpression of glycine-extended gastrin in transgenic mice results in increased colonic proliferation

“…The proliferative effect was 218% greater than that seen in wild-type mice, resulting in an increase in the thickness of the colonic mucosa along with colonic goblet cell hyperplasia of MTI/G-GLY mice when compared with wild-type mice. Goblet cell hyperplasia has been reported in other rodent models in which colonic proliferation has been induced (36,37).…”

Could Mycobacterium avium subspecies paratuberculosis cause Crohn’s disease, ulcerative colitis…and colorectal cancer?

“…While small intestinal goblet cell hyperplasia results from azoxymethane administration [ 68 ] and massive small intestinal resection [ 69 ], pathogenic bacteria and parasites are the only natural causes of intestinal goblet cell hyperplasia [ 70 , 71 ], including the protozoan parasite Giardia lamblia/intestinalis [ 72 ], the helminthes Trichinella spiralis [ 73 ] and Nippostrongylis brasiliensis [ 74 , 75 ], the bacteria Yersinia enterocolitica [ 76 ] and various Shigella species [ 77 ].…”