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PubMed1976

An ultrastructural study on precancerous and cancerous lesions of the glandular stomach in rats induced by N-methyl-N'-nitro-N-nitrosoguanidine.

Electron microscopic study was made on precancerous and cancerous lesions in glandular stomach of rats induced by MNNG. Three types of lesions, were found: regenerative glandular hyperplasia, adenomatous hyperplasia and adenocarcinoma. These were compared with the fine structure of similar lesions produced by X-irradiation in the glandular stomach of mice. The precancerous lesion in the present study demonstrated formation of adenomatous hyperplasia by epithelial cells which included mucoid cells characterized by sparce surface microvilli, a few erratic terminal webs, small number of mucous granules, many small mitochondria, and a bizarre nucleus. The development of these mucoid cells seems to be related with the growth of gastric carcinoma. The ultrastructure of adenocarcinomas revealed many structural variations or abnormalities of cellular differentiation. They were classified into 1) surface and pit mucous cell type, 2) pyloric gland cell type, 3) goblet cell type, 4) paneth cell type, 5) intestinal epithelial cell type, 6) endocrine cell type, 7) oncocyte type, 8) filament-rich cell type, and 9) anaplastic cell type involving intracellular microcyst cells. Filament-rich cells were found in poorly differentiated adenocarcinoma or scirrhous carcinoma and may be derived from metaplasia of tumor cell.

Adenocarcinoma↗
PubMed1977

Immunohistochemical identification of lysozyme in intestinal lesions in ulcerative colitis and Crohn's disease.

Lysozyme (LZM) was identified in ulcerative colitis in granulocytes, monocytes, and macrophages of the intestinal lamina propria. In contrast with findings in normal colon or rectum, in ulcerative colitis LZM was also detected in some mucosal crypt cells and metaplastic Paneth cells. In both ulcerative colitis and Crohn's disease LZM was present in inflammatory cells of crypt abscesses. In Crohn's disease intense LZM staining was seen in epitheloid cell granulomas. The present observations permit one explanation for the raised concentration of serum-LZM in patients with ulcerative colitis and Crohn's disease.

Colitis, Ulcerative↗
PubMed1985

Morphological range of hyperplastic polyps and carcinomas arising in hyperplastic polyps of the stomach.

A morphological range of 67 hyperplastic polyps was studied. They included polyps removed endoscopically and polyps found incidentally in resected stomachs with gastric ulcers and cancer. The hyperplastic polyps were essentially composed of cystic foveolae and pyloric type glands, lined by cells identical to those of the normal gastric mucosa. Thirty one polyps contained other cytological elements. In 18, intestinal metaplasia was seen; the tubules were mostly composed of columnar and goblet cells and lacked Paneth cells. In 11 polyps, nine cases of gastric dysplasia and two cases of intestinal dysplasia, dysplastic changes were found. The former consisted of a proliferation of irregularly shaped pits with pleomorphic cuboidal/columnar cells with relatively basophilic cytoplasm. They contained mucigen granules of a gastric type. The latter consisted of atypical pits composed of closely packed, tall columnar and small goblet cells, both resembling adenomatous cells of the colon. In three polyps carcinomas were seen, one of which was an intestinal type adenocarcinoma. In the other two, the cancer cells closely resembled the normal foveolar cells, containing gastric type mucigen granules. They were gastric type adenocarcinomas.

Adenocarcinoma↗
PubMed2006

Azoxymethane protects intestinal stem cells and reduces crypt epithelial mitosis through a COX-1-dependent mechanism.

Azoxymethane (AOM) is a potent DNA-damaging agent and carcinogen that induces intestinal and colonic tumors in rodents. Evaluation of the stem cell population by colony formation assay reveals that, within 8 h after treatment, AOM (10 mg/kg) elicited a prosurvival response. In wild-type (WT) mice, AOM treatment induced a 2.5-fold increase in intestinal crypt stem cell survival. AOM treatment increased stem cell survival in cyclooxygenase (COX)-2(-/-) but not COX-1(-/-) mice, confirming a role of COX-1 in the AOM-induced increase in stem cell survival. COX-1 mRNA and protein expression as well as COX-1-derived PGE(2) synthesis were increased 8 h after AOM treatment. Immunohistochemical staining of COX-1 demonstrated expression of the enzyme in the crypt epithelial cells, especially in the columnar epithelial cells between the Paneth cells adjacent to the stem cell zone. WT mice receiving AOM exhibited increased intestinal apoptosis and a simultaneous reduction in crypt mitotic figures within 8 h of injection. There were no significant differences in baseline or AOM-induced intestinal epithelial apoptosis between WT and COX-1(-/-) mice, but there was a complete reversal of the AOM-mediated reduction in mitosis in COX-1(-/-) mice. This suggests that COX-1-derived PGE(2) may play a key role in the early phase of intestinal tumorigenesis in response to DNA damage and suggests that COX-1 may be a potential therapeutic target in this model of colon cancer.

Animals↗
PubMed2007

Protection of the neonate by the innate immune system of developing gut and of human milk.

The neonatal adaptive immune system, relatively naïve to foreign antigens, requires synergy with the innate immune system to protect the intestine. Goblet cells provide mucins, Paneth cells produce antimicrobial peptides, and dendritic cells (DCs) present luminal antigens. Intracellular signaling by Toll-like receptors (TLRs) elicits chemokines and cytokines that modulate inflammation. Enteric neurons and lymphocytes provide paracrine and endocrine signaling. However, full protection requires human milk. Breast-feeding reduces enteric infection and may reduce chronic disease in later life. Although human milk contains significant secretory immunoglobulin A (sIgA), most of its protective factors are constitutively expressed. Multifunctional milk components are nutrients whose partial digestion products inhibit pathogens. Cytokines, cytokine receptors, TLR agonists and antagonists, hormones, anti-inflammatory agents, and nucleotides in milk modulate inflammation. Human milk is rich in glycans (complex carbohydrates): As prebiotics, indigestible glycans stimulate colonization by probiotic organisms, modulating mucosal immunity and protecting against pathogens. Through structural homology to intestinal cell surface receptors, glycans inhibit pathogen binding, the essential first step of pathogenesis. Bioactive milk components comprise an innate immune system of human milk whereby the mother protects her nursing infant. Interactions between human milk glycans, intestinal microflora, and intestinal mucosa surface glycans underlie ontogeny of innate mucosal immunity, pathobiology of enteric infection, and inflammatory bowel diseases.

Gastrointestinal Tract↗
PubMed2005

[Acinic cell-like differentiation in invasive ductal carcinoma and in ductal hyperplasia of the breast--report of two cases].

Described are two epithelial lesions of the breast displaying extremely rare, widespread acinic cell-like differentiation (metaplasia). Two women, 70 and 40-year-old, one with invasive ductal papillocarcinoma, the other one with conventional intraductal hyperplasia without atypia, both demonstrated massive diffuse, PAS positive, granular eosinophilic transformation of the cell cytoplasm. This unusual cell appearance closely simulated acinar cells in normal serous salivary gland/acinic cell carcinoma or Paneth cells. Both extensive expression of lysozyme and finding of numerous zymogen granules ultrastructurally confirmed the acinic cell-like fenotype. Discussed is differential diagnosis of the breast neoplasm containing overt eosinophilic and granular cytoplasm. Reviewing literature and comparing our unique finding of unusual salivary-type differentiation in conventional ductal hyperplasia of the breast, biologic implications are considered.

Adult↗
PubMed1976

Gross, microscopic and ultrastructural study of the intestinal tube of Xenodon merremii Wagler, 1824 (Ophidia).

The small and large intestines of Xenodon merremii have a similar structure. They are separated by a sphincter of thickened circular muscle. The mucosa of the proximal part of the small intestine is raised into a honeycomb pattern, but distally there are only longitudinal folds. The lining epithelium throughout is of a simple columnar type, with absorptive, goblet, argentaffin and argyrophil cells, but no Paneth cells, villi or crypts of Lieberkühn are present.

Animals↗
PubMed1995

[Antimicrobial oligopeptides--an important factor in non-specific defense against infection].

For survival of plants, animals as well as main in a nature full of aggressive microbes, endogenous antibiotics play an essential role, which is not yet fully appreciated in medicine and science. For example in the granules of polymorphonuclear granulocytes and macrophages or even of specialized epithelial cells such as Paneth cells in the crypts of the intestinal mucosa, oligopeptides are produced with a wide range of antimicrobial activity. According to their chemical structures and modes of action they can be grouped into various different families. The physiological role of these agents on the surface of skin and mucosa or within host tissue is only incompletely understood.

Bacteria↗
PubMed2000

Distribution of group II phospholipase A2 protein and mRNA in rat tissues.

Group II phospholipase A2 (PLA2) is an acute-phase protein and an important component of the host defense against bacteria. In this study we investigated the distribution of PLA2 protein by immunohistochemistry and the distribution of mRNA of PLA2 by Northern blotting and in situ hybridization in rat tissues. PLA2 protein was localized in the Paneth cells of the intestinal mucosa, chondrocytes and the matrix of cartilage, and megakaryocytes in the spleen. By Northern blotting, mRNA of PLA2 was found in the gastrointestinal tract, lung, heart, and spleen. By in situ hybridization, PLA2 mRNA was localized in the Paneth cells of the small intestinal mucosa but in no other cell types. Our results show specific distribution of PLA2 in a limited number of cell types in rat tissues. The reagents developed in this study (the anti-rat PLA2 antibody and probes for Northern blotting and in situ hybridization of mRNA of rat PLA2) will provide useful tools for future studies concerning the role of PLA2 in various experimental disease models.

Amino Acid Sequence↗
PubMed1991

Expression of enhancing factor gene and its localization in mouse tissues.

Enhancing factor (EF), a 14 kDa protein, isolated from mouse small intestines, has been reported from this laboratory. Based on our earlier studies EF has been implicated in cell proliferation. Preliminary immunohistochemical studies have shown EF to be localized in the Paneth cells of small intestines. In this paper we report the tissue distribution of EF using conditions optimized for immunohistochemical staining. In addition, the data are supported by northern blot analysis using a nick translated cDNA probe specific for EF. The results indicate that EF gene is actively transcribed mainly in the intestines. The chief source of synthesis of EF appears to be the Paneth cells located at the base of the crypts of Lieberkühn.

Animals↗
PubMed1994

Duodenal adenomas in familial adenomatous polyposis: relation of cell differentiation and mucin histochemical features to growth pattern.

We performed a clinicopathologic analysis of 74 periampullary and duodenal adenomas from 30 patients with familial adenomatous polyposis to evaluate the growth pattern, mucin histochemical profile, and degree and significance of Paneth cell and endocrine cell differentiation in these lesions. A trend toward more numerous adenomas was seen in patients with the longest intervals since their previous colectomies. Adenomas were most often clustered in the periampullary region and were numerous (> 20) in 40% of patients. Periampullary and duodenal adenomas were morphologically similar; both exhibited the same size-villous shape-dysplasia relationship as sporadic and familial adenomatous polyposis-associated colonic adenomas. Adenomas showed a heterogenous pattern of mucin production (mixed small intestinal-large intestinal types), with a shift toward the colonic type (sulfomucin) in lesions that were larger, villous, or severely dysplastic. Ninety-two percent of adenomas showed Paneth cell differentiation (average n Paneth cells/high power field = 24.5), and 99% showed endocrine cell differentiation (average n endocrine cells/high power field = 64.4). In general, the proportion of these specialized cell types was inversely related to size, villous shape, and degree of epithelial dysplasia. These results suggest that periampullary and duodenal adenomas in familial adenomatous polyposis arise from the neoplastic transformation of an undifferentiated stem cell that retains its ability for multidirectional differentiation.

Adenoma↗
PubMed1982

Tissue uptake of zinc in rats following the administration of zinc dipicolinate or zinc histidinate.

Tissue uptake of zinc was determined in rats fed a low zinc diet (less than 1 ppm Zn) and an adequate zinc diet (20 ppm Zn) following the intramuscular injection of either zinc dipicolinate (ZnPA2) or zinc histidinate (ZnHis). Significant differences were observed when dietary and treatment effects on zinc uptake were compared in pancreas, duodenum, jejunum, ileum, kidney, and liver. Zinc uptake by the pancreas was higher in rats fed adequate zinc than in rats fed low zinc regardless of which zinc complex was injected, suggesting that the pancreas has a role in zinc excretion. Since ZnHis was more readily taken up than ZnPA2 by the pancreas of rats on the zinc-adequate diet, zinc chelated by histidine may be more readily excreted than zinc chelated by picolinic acid. No differences in zinc uptake were observed in the intestinal segments from rats fed low zinc compared to rats fed adequate zinc. However, in rats fed low zinc, ZnPA2 was more readily taken up than ZnHis by all intestinal segments implying that zinc chelated by picolinic acid may be more available for storage or utilization by the small intestine than zinc chelated by histidine. Also, the ileum had the highest zinc uptake regardless of which zinc complex was injected. Since the ileum has the largest population of Paneth cells, and high zinc uptake observed in this segment of the small intestine suggests a role for Paneth cells in zinc homeostasis.

Animals↗
PubMed1975

[Acrodermatitis enteropathica--a disturbance of zinc metabolism with zinc malabsorption (author's transl)].

The intestinal resorption of zinc using 65ZnCl2 was estimated in 3 patients with acrodermatitis enteropathica, 2 healthy controls, and 3 heterozygotes. After oral application of 65Zn the whole body activity was measured by a whole body counter for 34 days. The 65Zn resorption of the patients amounted to 16, 42 and 30% of the applied dose, whereas the resorption values of the heterozygotes and the controls were in the range of 58 and 77%. The elimination of 65Zn from the body amounted to about 0.7% of the applied dose with no difference between controls and patients with acrodermatitis enteropathica. Before therapy the serum-zinc levels of patients were markedly decreased. After oral application of high doses of zinc aspartate (2 times 400 mg/day) all clinical symptoms disappeared within a week. The results point at a causal connection between zinc and the pathogenesis of acrodermatitis enteropathica. Ultrastructural alterations of the Paneth cells of the intestines are also shown in this disease [12] as have also been seen in Paneth cells of zinc deficient rats [Beitr. Path. 145, 336 (1972)].

Acrodermatitis↗
PubMed1979

Ultrastructural features of spironucleosis (hexamitiasis) in x-irradiated rat small intestine.

An alteration in the host response to the intestinal protozoan Spironucleus (Hexamita) muris was noted in x-irradiated rat small intestine. When few were present in the crypt lumina, the intestinal microvillar border was normal. However, when larger numbers were present, the microvilli were greatly reduced in numbers or entirely absent in some regions. The organism was identified in the base of the crypt lumen, in apical portions of mucous cells, and near the basement membrane. Spironucleus enclosed by digestive vacuoles occasionally appeared to be in the process of being extruded through the basement membrane. Not all intracellular protozoa were surrounded by such digestive vacuoles. Spironucleus was never seen in association with the digestive vacuoles of Paneth cells. Since it has been suggested that Paneth cells have a role as a fixed phagocyte, ingesting protozoa and other microorganisms, the results presented here suggest that this function may have been impaired in irradiated animals.

Animals↗
PubMed2006

Rapid expansion of intestinal secretory lineages following a massive small bowel resection in mice.

Following massive small bowel resection (SBR) in mice, there are sustained increases in crypt depth and villus height, resulting in enhanced mucosal surface area. The early mechanisms responsible for resetting and sustaining this increase are presently not understood. We hypothesized that expansion of secretory lineages is an early and sustained component of the adaptive response. This was assessed in the ileum by quantitative morphometry at 12 h, 36 h, 7 days, and 28 days and by quantitative RT-PCR of marker mRNAs for proliferation and differentiated goblet, Paneth cell, and enterocyte genes at 12 h after 50% SBR or sham operation. As predicted, SBR elicited increases of both crypt and villus epithelial cells, which were sustained though the 28 days of the experiment. Significant increases in the overall number and percentage of both Paneth and goblet cells within intestinal epithelium occurred by 12 h and were sustained up to 28 days after SBR. The increases of goblet cells after SBR were initially observed within villi at 12 h, with marked increases occurring in crypts at 36 h and 7 days. Consistent with this finding, qRT-PCR demonstrated significant increases in the expression of mRNAs associated with proliferation (c-myc) and differentiated goblet cells (Tff3, Muc2) and Paneth cells (lysozyme), whereas mRNA associated with differentiated enterocytes (sucrase-isomaltase) remained unchanged. From these data, we speculate that early expansion of intestinal secretory lineages within the epithelium of the ileum occurs following SBR, possibly serving to amplify the signal responsible for initiating and sustaining intestinal adaptation.

Anastomosis, Surgical↗
PubMed1988

Is epidermal growth factor involved in development of duodenal polyps in familial polyposis coli?

Duodenal adenomas are a frequent extracolonic manifestation in patients with familial polyposis coli (FPC). Epidermal growth factor (EGF), a polypeptide that stimulates cellular growth and differentiation, is localized in Paneth cells in the small intestine. In two patients with FPC, we found EGF immunoreactivity in duodenal adenomas. Numerous EGF immunoreactive Paneth cells were localized, not as usually, in the bottom of the crypts, but scattered along the crypts alone or in clusters. We do not know whether EGF is involved in the development of duodenal polyps in FPC patients, or whether the present findings represent secondary changes in duodenal polyps.

Adenoma↗
PubMed1996

Patterns of gene expression along the crypt-villus axis in mouse jejunal epithelium.

BACKGROUND: There is considerable interest in gene expression along the crypt-villus axis of the small intestinal epithelium, particularly in the identification of genes expressed in intestinal crypts. METHODS: In an attempt to identify crypt-expressed genes, single-stranded cDNA made from normal mouse jejunal epithelium was used in subtractive hybridization against single-stranded cDNA from epithelium from which crypt cells were depleted by 2,000 rads of gamma irradiation. Partial DNA sequence and in situ hybridization of 72 resulting clones were determined. RESULTS: The sequence of 45 clones matched previously published genes. Gene expression patterns fell into three categories: expression throughout the crypt-villus axis, expression restricted to the villus, and expression restricted to the crypt. Clones in the first two categories could be further divided into three subgroups: those with uniform expression, those with an increasing gradient of expression, and those with a decreasing gradient of expression along the crypt-villus axis. Twenty two clones showed a stronger expression in crypt and lower villus cells, four of these were differentially localized to the crypt. Two of the crypt localized clones were uniformly expressed throughout the crypt, expression of one was stronger in the lower crypt, and expression of the remaining clone was enhanced Paneth cells. We report the full-length cDNA sequence of the Paneth-cell-enhanced clone. CONCLUSIONS: The screen isolated crypt-expressed genes that may prove useful tools in the study of crypt biology. In a companion report, we characterize one of the crypt clones.

Amino Acid Sequence↗
PubMed2006

Foxl1-deficient mice exhibit aberrant epithelial cell positioning resulting from dysregulated EphB/EphrinB expression in the small intestine.

The winged helix transcription factor Foxl1, expressed in the gut mesenchyme, regulates epithelial cell proliferation and differentiation through the Wnt/beta-catenin pathway. To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice. The small intestine of Foxl1-deficient mice manifested aberrant crypt structure, including widely distributed Paneth cells, which coincided with the ectopic and increased expression of EphB2 and EphB3, which are key regulators of epithelial cell positioning. Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. Such an increase in Wnt expression was remarkable in the mesenchyme, where the aberrant Paneth cell positioning was observed by in situ hybridization. Foxl1 plays an important role in the maintenance of crypt architecture and epithelial cell positioning through the mesenchymal-epithelial interaction in the small intestine. This interaction is essential for the normal regulation of the Wnt/beta-catenin pathway and the subsequent EphB/EphrinB expression.

Animals↗