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At least 469 records · Page 26Linked to original sources
PubMed2004

Global gene expression analysis of rat colon cancers induced by a food-borne carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.

Colon cancers develop after accumulation of multiple genetic and epigenetic alterations in colon epithelial cells. To shed light on global changes in gene expression of colon cancers and to gain further insight into the molecular mechanisms underlying colon carcinogenesis, we have conducted a comprehensive microarray analysis of mRNA using a rat colon cancer model with the food-borne carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Of 8749 genes or ESTs on a high density oligonucleotide microarray, 27 and 46 were over- and underexpressed, respectively, by > or =3-fold in colon cancers in common in two rat strains with distinct susceptibility to PhIP carcinogenesis. For example, genes involved in inflammation and matrix proteases and a cell cycle regulator gene, cyclin D2, were highly expressed in colon cancers. In contrast, genes encoding structural proteins, muscle-related proteins, matrix-composing and mucin-like proteins were underexpressed. Interestingly, a subset of genes whose expression is characteristic of Paneth cells, i.e. the defensins and matrilysin, were highly overexpressed in colon cancers. The presence of defensin 3 and defensin 5 transcripts in cancer cells could also be confirmed by in situ mRNA hybridization. Furthermore, Alcian blue/periodic acid Schiff base (AB-PAS) staining and immunohistochemical analysis with an anti-lysozyme antibody demonstrated Paneth cells in the cancer tissues. AB-PAS-positive cells were also observed in high grade dysplastic aberrant crypt foci, which are considered to be preneoplastic lesions of the colon. Our results suggest that Paneth cell differentiation in colon epithelial cells could be an early morphological change in cryptic cells during colon carcinogenesis.

Alcian Blue↗
PubMed1977

Acrodermatitis enteropathica. II. Zinc deficiency and ultrastructural findings.

The basic defect in acrodermatitis enteropathica (A.E.) is zinc deficiency caused by zinc malabsorption. The clinical symptoms disappear and serum zinc levels normalize after oral treatment with zinc. A report is given on two siblings suffering from A.E., both treated with oxyquinolines for a long period with changing clinical success. A permanent clinical remission could be achieved by treatment with zinc-sulphate at doses of 110-220 mg daily. The serum zinc levels normalized. The correlation between the zinc concentration of the hair and the kind of therapy was not very close. As we have shown in our first communication, the Paneth cells of the intestinal mucosa display ultrastructural changes in form of an unhomogeneous structure of the cytoplasm, formation of giant granules, and inclusion bodies. The zinc-therapy led to a complete normalization of the pathological changes in the Paneth cells. Thus, the changes in the Paneth cells in A.E. are the result and not the cause of zinc deficiency.

Acrodermatitis↗
PubMed1997

Gene expression of group II phospholipase A2 in intestine in ulcerative colitis.

BACKGROUND: It has been suggested that phospholipase A2 (PLA2) has an essential role in the pathogenesis of inflammatory bowel diseases. AIMS: This study aimed at identifying cells in intestinal and mesenteric tissue samples that might express group II phospholipase A2 (PLA2-II) at the mRNA and enzyme protein levels in patients with ulcerative colitis. PATIENTS AND TISSUE SAMPLES: Tissue samples were obtained from the intestine, mesentery, skeletal muscle, and subcutaneous fat of six patients who underwent panproctocolectomy for severe ulcerative colitis. Mucosal biopsy specimens were obtained from the colon of another group of six patients with ulcerative colitis during routine diagnostic colonoscopies. Tissues from six patients without intestinal inflammatory diseases served as controls. METHODS: Tissue samples were studied by light microscopy, immunohistochemistry for PLA2-II enzyme protein, and in situ hybridisation and northern hybridisation for PLA2-II mRNA. RESULTS: PLA2-II mRNA and PLA2-II protein were detected in metaplastic Paneth cells in six patients and in the columnar epithelial cells of colonic mucosa in four out of six patients with active ulcerative colitis. Positive findings were less numerous in patients with mild ulcerative colitis. Only two out of six control patients had a weak positive signal for PLA2-II mRNA and one of these two patients had a weak positive immunoreaction for PLA2-II in columnar epithelial cells in the colonic mucosa. None of the control patients had metaplastic Paneth cells. CONCLUSIONS: Metaplastic Paneth cells and colonic epithelial cells synthesise PLA2-II in ulcerative colitis. The activity of the PLA2-II synthesis seems to be related to the degree of inflammation in the diseased bowel.

Adult↗
PubMed1994

Mucin-secreting adenocarcinoma of the prostate with neuroendocrine differentiation and Paneth-like cells.

We present an unusual variant of prostatic adenocarcinoma with obvious mucinous and neuroendocrine features, arising in the transition zone. The neuroendocrine component is largely represented by Paneth-like cells (PLCs). These cells correspond to previously described eosinophilic cells and are amphicrine. We could demonstrate immunohistochemically the presence of calcitonin in some of these PLCs. The prognostic significance of these special characteristics is not well known, but it is most likely that this type of prostate cancer will not respond well to hormonal therapy.

Adenocarcinoma, Mucinous↗
PubMed2002

Protection of the Peyer's patch-associated crypt and villus epithelium against methotrexate-induced damage is based on its distinct regulation of proliferation.

The crypt and villus epithelium associated with Peyer's patches (PPs) is largely spared from methotrexate (MTX)-induced damage, compared with the non-patch (NP) epithelium. To assess the mechanism(s) preventing damage to the PP epithelium after MTX treatment, epithelial proliferation, apoptosis, and cell functions were studied in a rat-MTX model. Small intestinal segments containing PPs were excised after MTX treatment. Epithelial proliferation and apoptosis were assessed by detection of incorporated BrdU and cleaved caspase-3, respectively. Epithelial functions were determined by the expression of cell type-specific gene products at mRNA and protein level. Before and after MTX treatment, the number of BrdU-positive cells was higher in PP crypts than in NP crypts. BrdU incorporation was diminished in NP crypts, while in PP crypts incorporation was hardly affected. In PP and NP crypts, similar and increased levels of cleaved caspase-3-positive cells were observed after MTX. The enterocyte markers, sucrase-isomaltase, sodium-glucose co-transporter 1, glucose transporters 2 and 5, and intestinal and liver fatty acid binding protein, were down-regulated after MTX in NP epithelium but not in PP epithelium. In contrast, expression of the goblet cell markers, Muc2 and trefoil factor 3, and the Paneth cell marker, lysozyme, was maintained after MTX in both PP and NP epithelium. In conclusion, as MTX-induced apoptosis was similar in PP and NP crypts, the protection of the PP epithelium seems to be based on differences in the regulation of epithelial proliferation. Enterocyte function in the PP epithelium was unaffected by MTX treatment. Goblet and Paneth cell function was maintained in both NP and PP epithelium.

Animals↗
PubMed1978

Experimentally induced intestinal metaplasia in Wistar rats by X-ray irradiation.

The gastric region of 5-week-old female Wistar rats was irradiated daily with 500 rad of X-ray up to a total of six times. Goblet cells and marker enzymes of the small intestine, such as lactase, trehalase, and maltase, appeared in the pyloric region of the glandular stomach of the rats from the 1st week after final irradiation. Intestinal type crypt without Paneth cells was observed from the 8th week. Sucrase activity appeared from the 26th week. Intestinal metaplasia with Paneth cells appeared from the 71st week. The number of goblet cells, intestinal type crypts, and Paneth cells increased with age. Gastric adenocarcinoma did not develop after irradiation.

Animals↗
PubMed1995

Synchronous cancers of the esophagus and the ampulla of Vater after distal gastrectomy: successful removal of the esophagus, gastric remnant, duodenum, and pancreatic head.

A case of synchronous squamous cell carcinoma of the esophagus and adenocarcinoma of the ampulla of Vater after previous gastrectomy is presented. The coexistence of these two lesions has never been reported in the English literature. We performed a subtotal esophagectomy, total residual gastrectomy, and pancreaticoduodenectomy with lymph node dissection in a one-stage procedure. An operation of this magnitude could be safely performed with attention to meticulous surgical technique and intensive postoperative care. Histological examination of the ampulla lesion showed adenocarcinoma with Paneth-cell differentiation. This is a rare lesion, and a review of the literature revealed only one other case. Neoplastic Paneth cells were also found in lymph node metastasis that originated from the ampulla tumor. This case confirms that cells with Paneth-cell differentiation can be a significant component in invasive carcinoma.

Adenocarcinoma↗
PubMed2005

Differential labeling by monoclonal antibodies Adnab-9 and anti-alpha-defensin 5 based on the distribution and adenomatous tissue content of colonic polyps.

We sought a correlation between site and morphology of colonic polyps by labeling with neoplastic and general Paneth cell markers, monoclonal antibodies Adnab-9 and anti-alpha-defensin 5, respectively. Proportions labeled by Adnab-9 and anti-alpha-defensin 5 were, respectively, 42 and 85% for adenomas, 39 and 63% for early tubular adenomas, 41 and 44% for serrated, 34 and 20% for mixed, and 11 versus 2.7% for hyperplastic polyps. Compared with hyperplastic polyps, the proportion of other polyps labeled by Adnab-9 or anti-alpha-defensin 5 was higher but this difference was more significant for distal (P = 0.008 for Adnab-9 and P = 0.0001 for anti-alpha-defensin 5) than proximal (P = 0.645 and P = 0.154, respectively) polyps. While increased labeling of all proximal polyps compared to distal ones mirrored the colonic distribution of Paneth cells, distal adenomas tended to have a higher proportion labeled by Adnab-9, suggesting that Adnab-9 labels Paneth cells associated with increased neoplastic potential.

Adenomatous Polyps↗
PubMed2003

Molecular features of adult mouse small intestinal epithelial progenitors.

The adult mouse small intestinal epithelium undergoes perpetual regeneration, fueled by a population of multipotential stem cells and oligopotential daughters located at the base of crypts of Lieberkühn. Although the morphologic features of small intestinal epithelial progenitors (SiEPs) are known, their molecular features are poorly defined. Previous impediments to purification and molecular characterization of SiEPs include lack of ex vivo clonigenic assays and the difficulty of physically retrieving them from their niche where they are interspersed between their numerous differentiated Paneth cell daughters. To overcome these obstacles, we used germ-free transgenic mice lacking Paneth cells to obtain a consolidated population of SiEPs with normal proliferative activity. These cells were harvested by laser capture microdissection. Functional genomics analysis identified 163 transcripts enriched in SiEPs compared with Paneth cell-dominated normal crypt base epithelium. The dataset was validated by (i) correlation with the organellar composition of SiEPs versus Paneth cells, (ii) similarities to databases generated from recent mouse hematopoietic and neural stem cell genome anatomy projects, and (iii) laser capture microdissectionreal-time quantitative RT-PCR studies of progenitor cell-containing populations retrieved from the small intestines, colons, and stomachs of conventionally raised mice. The SiEP profile has prominent representation of genes involved in c-myc signaling and in the processing, localization, and translation of mRNAs. This dataset, together with our recent analysis of gene expression in the gastric stem cell niche, discloses a set of molecular features shared by adult mouse gut epithelial progenitors.

Animals↗
PubMed1997

Immunohistochemical localization of cysteine-rich intestinal protein in rat small intestine.

Cysteine-rich intestinal protein (CRIP) is a LIM (cysteine-rich motif of leu-11, isl-1, and mec-3 genes) domain protein with a double zinc finger motif. The protein is abundantly expressed in the intestine, peritoneal macrophages, and peripheral blood mononuclear cells. The function of CRIP is not known. The purpose of this study was to determine the cellular distribution of CRIP in rat intestine, as an initial step toward eventual determination of a function. Immunohistochemical and immunogold labeling electron microscopy using a purified polyclonal rabbit antibody to a synthetic peptide representing a zinc finger domain of rat CRIP were carried out on sections of rat duodenum. Western blotting was used to detect signal specificity of the antibodies. These immunohistochemical and electron microscopy studies showed particularly high abundance of CRIP in the cytoplasmic granules of Paneth cells of the intestine. Some evidence of CRIP expression was also found in cells of the villus tip, but abundance was less than that found in the Paneth cells. The localization of CRIP in Paneth cells and its presence in mononuclear cells suggests that CRIP may be involved in host defense mechanisms and/or tissue differentiation/remodeling processes common to these cell types.

Animals↗
PubMed1992

Lysozyme gene expression in inflammatory bowel disease.

Riboprobe in situ hybridization (rISH) demonstrates active lysozyme synthesis in ulcerative colitis and Crohn's disease. Maximal labeling was seen in Paneth cells, macrophages, and granulomas. Diffuse infiltration of the mucosa by lysozyme-rich polymorphs characterizes ulcerative colitis but obscures reactivity in other cell lineages in immunohistochemical studies; lysozyme mRNA is not detected in polymorphs, rISH giving a clearer picture than immunohistochemical studies of the active synthesis of lysozyme within the gut in inflammatory bowel disease. In ulcerative colitis, strong signals localized to Paneth cell metaplasia were found in 11 of 20 cases and to a lesser degree in non-Paneth cell lineages in regenerative mucosa in 13 of 20 cases. In Crohn's disease, abundant labeling was seen in tuberculoid granulomas (5 of 20) and over macrophage aggregates in the lamina propria in another 7, characteristic patterns not encountered in ulcerative colitis. Low levels of lysozyme messenger RNA were found in the ulceration-associated cell lineage ("pseudopyloric metaplasia"). These results support the view that neutrophils are largely responsible for elevated fecal lysozyme levels in ulcerative colitis and macrophages for elevated serum lysozyme levels in Crohn's disease.

Colitis, Ulcerative↗
PubMed1979

Comparative effects of CCK-PZ on certain intestinal hydrolases in the mucosa and in the luminal content of the hamster jejuno-ileum.

After isolation of the hamster small intestine, the effects of a continuous infusion of cholecystokinin-pancreozymin (CCK-PZ) are studied. Several enzymic activities are measured in the intestinal lumen and compared with the level found in the intestinal homogenate. During CCK-PZ infusion we observed a direct stimulation of Paneth cells associated with an increase of lysozyme activity. Furthermore this work confirms the stimulating effect of CCK-PZ on alkaline phosphatase and amino-peptidase. Maltase and sucrase levels were unaffected. The liberation of the hydrolase of the brush border in the intestinal lumen is negligible and cannot be considered as a true secretion. Only granule content of Paneth cells is actually secreted. However, biochemical data, corroborated by morphological results, suggest that Paneth cell secretion could in part be absorbed on the outer surface of the brush border.

Alkaline Phosphatase↗
PubMed1994

Carcinoid tumour complicating inflammatory bowel disease. A study of two cases with review of the literature.

Two cases of carcinoid tumour complicating inflammatory bowel disease (IBD) are presented. Both tumours were located in the appendiceal tip. The first case occurred in a man with Crohn's disease (CD), and the second one in a woman suffering from ulcerative colitis (UC). Histochemical and immunohistochemical studies were not allowed on case 1 because the tumour was not still present on serial sections of the appendix. On case 2, tumour cells were not reactive with Grimelius and Masson-Fontana stainings, but were strongly stained with anti-keratin and anti-chromogranin monoclonal antibodies (MAb), and faintly expressed neuron specific enolase (NSE), and Leu-7. Both cases occurred in inflammatory or damaged mucosa which exhibited Paneth cell metaplasia and hyperplasia and areas indefinite for dysplasia. Along with these lesions, hyperplasia of enteroendocrine cells was pointed out in the neighbouring appendiceal and colonic mucosa by means of anti-chromogranin MAb. These data suggest that the association of carcinoid tumour with IBD, albeit rare, is not coincidental and is the result of hyperplastic and dysplastic troubles that may involve enteroendocrine cells as well as such other derivatives of digestive stem cells as columnar cells, goblet cells and Paneth cells.

Adult↗
PubMed2000

Proliferative populations in intestinal metaplasia: evidence of deregulation in Paneth and goblet cells, but not endocrine cells.

In the small intestinal mucosa, four principal epithelial cell lineages are found - the Paneth, goblet, enterocytic, and endocrine cell lineages. These cell lineages are terminally differentiated, non-proliferative, and derive from multipotent stem cells near the bases of the crypts of Lieberkühn. Intestinal metaplasia of the stomach is considered to be a premalignant condition. Since proliferative populations in this condition are not well studied, this feature was examined using double-labelling immunohistochemical and histochemical methods; 20 paraffin blocks of small intestinal mucosa and 24 paraffin blocks of intestinal metaplasia of the human stomach were studied. Double-staining was carried out with MIB-1 as a proliferation marker, with Alcian blue for goblet cells, anti-chromogranin A for endocrine cells, and p-dimethylaminobenzaldehyde-nitrite for Paneth cells. Double-labelling showed that numerous Paneth cells and goblet cells in intestinal metaplasia were in the cell cycle, but endocrine cells appeared non-proliferative. Double-labelled Paneth or endocrine cells were not seen in the control small intestinal mucosa but scanty double-labelled goblet cells were observed in normal intestinal mucosa. In intestinal metaplasia of the stomach, there is evidence of cell-cycle deregulation in the goblet and Paneth cell lineages. These observations have considerable implications for the biology and histogenesis of Paneth cells, goblet cells, and endocrine cells, and the nature of intestinal metaplasia in the gastric mucosa.

Cell Division↗
PubMed2002

Specific responses in rat small intestinal epithelial mRNA expression and protein levels during chemotherapeutic damage and regeneration.

The rapidly dividing small intestinal epithelium is very sensitive to the cytostatic drug methotrexate. We investigated the regulation of epithelial gene expression in rat jejunum during methotrexate-induced damage and regeneration. Ten differentiation markers were localized on tissue sections and quantified at mRNA and protein levels relative to control levels. We analyzed correlations in temporal expression patterns between markers. mRNA expression of enterocyte and goblet cell markers decreased significantly during damage for a specific period. Of these, sucrase-isomaltase (-62%) and CPS (-82%) were correlated. Correlations were also found between lactase (-76%) and SGLT1 (-77%) and between I-FABP (-52%) and L-FABP (-45%). Decreases in GLUT5 (-53%), MUC2 (-43%), and TFF3 (-54%) mRNAs occurred independently of any of the other markers. In contrast, lysozyme mRNA present in Paneth cells increased (+76%). At the protein level, qualitative and quantitative changes were in agreement with mRNA expression, except for Muc2 (+115%) and TFF3 (+81%), which increased significantly during damage, following independent patterns. During regeneration, expression of each marker returned to control levels. The enhanced expression of cytoprotective molecules (Muc2, TFF3, lysozyme) during damage represents maintenance of goblet cell and Paneth cell functions, most likely to protect the epithelium. Decreased expression of enterocyte-specific markers represents decreased enterocyte function, of which fatty acid transporters were least affected.

Animals↗
PubMed2005

Defence molecules in intestinal innate immunity against bacterial infections.

PURPOSE OF REVIEW: Antimicrobial proteins are key effector molecules of innate immunity. The review discusses recent progress in understanding the function of these host defence molecules in intestinal physiology. RECENT FINDINGS: All antimicrobial proteins can inhibit or kill bacteria in vitro, but differ markedly in their localization, regulation, and additional activities. alpha-Defensins are expressed constitutively in human neutrophils and small intestinal Paneth cells, where they require proteolytic processing and signal-induced release to be active in the intestinal lumen. Neutrophil-derived alpha-defensins can inhibit angiogenesis. Cryptdin-related sequence peptides form a subfamily of alpha-defensins in murine but not human Paneth cells that can form covalently linked heterodimers, leading to increased structural diversity and antimicrobial target range. Human beta-defensins (hBD) are expressed prominently in epithelial cells of the intestinal tract and other organs exposed to the environment. Their epithelial production is either constitutive, as exemplified by hBD-1, or strongly inducible, as shown for hBD-2,-3, and -4. Human cathelicidin, LL-37/hCAP18, is expressed constitutively by differentiated epithelial cells in the colon and stomach, but not the small intestine, as well as neutrophils and mast cells. It has multiple functions beyond its antimicrobial activity, including promotion of angiogenesis, attraction of leukocyte subsets, and activation of chemokine secretion. Angiogenins are a family of host defence-related ribonucleases, of which at least one is secreted by murine Paneth cells. SUMMARY: The differential expression of diverse antimicrobial proteins in the gastrointestinal tract suggests that they occupy distinct functional niches in mucosal innate defence, which holds promise for pharmacological exploitation of their antimicrobial properties.

Animals↗