scholarly journals Phenotypic and functional characterisation of myofibroblasts, macrophages, and lymphocytes migrating out of the human gastric lamina propria following the loss of epithelial cells

Gut ◽  
1999 ◽  
Vol 44 (3) ◽  
pp. 323-330 ◽  
Author(s):  
K C Wu ◽  
L M Jackson ◽  
A M Galvin ◽  
T Gray ◽  
C J Hawkey ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Basement Membrane ◽  
Lamina Propria ◽  
Surface Epithelium ◽  
Prostaglandin E ◽  
Tissue Samples ◽  
Membrane Pores ◽  
Functional Characterisation ◽  
Polymerase Chain ◽  
Cox 1

BACKGROUNDThe basement membrane of human colonic mucosa contains numerous discrete pores. We have recently shown that following loss of the surface epithelium, many cells migrate out of the colonic lamina propria via basement membrane pores.AIMSTo characterise cells migrating out via basement membrane pores of the human gastric lamina propria, following loss of the surface epithelium.METHODSFresh human gastric mucosal samples were completely denuded of epithelial cells and placed in culture. Tissue samples were studied by electron microscopy (EM) and cells by EM, FACS analysis, immunohistochemistry, and reverse transcription polymerase chain reaction (RT-PCR).RESULTSEM showed numerous discrete pores (0.65–8.29 μm in diameter) in the subepithelial basement membrane. During culture of mucosal samples denuded of epithelial cells, lymphocytes, macrophages, and myofibroblasts migrated out of the lamina propria via the basement membrane pores. The lymphocytes were predominantly CD45RO+ and CD69+ T cells. Macrophages were shown to express cyclooxygenase (COX) 1 and 2 enzymes. Myofibroblasts were established in culture and, despite prolonged culture and passage, retained their phenotype. They expressed mRNA and protein for COX 1 and 2 enzymes and their release of prostaglandin E2 was inhibited by selective COX 1 and 2 inhibitors.CONCLUSIONSLamina propria cells migrating out of cultured denuded gastric mucosal samples have been characterised phenotypically and functionally. Such cells would be suitable for studies of their interactions with epithelial cells and also with Helicobacter pylori and its products.

scholarly journals Are there attacking points in the eicosanoid cascade for chemotherapeutic options in benign meningiomas?

2007 ◽  
Vol 23 (4) ◽  
pp. E8 ◽  
Author(s):  
Christina Pfister ◽  
Rainer Ritz ◽  
Heike Pfrommer ◽  
Antje Bornemann ◽  
Marcos S. Tatagiba ◽  
...  
Keyword(s):  
World Health ◽  
Pcr Analysis ◽  
Prostaglandin E ◽  
Tissue Samples ◽  
Human Cortex ◽  
Normal Human ◽  
Cox 2 ◽  
Cox 1

Object The current treatment for recurrent or malignant meningiomas with adjuvant therapies has not been satisfactory, and there is an intense interest in evaluating new molecular markers to act as therapeutic targets. Enzymes of the arachidonic acid (AA) cascade such as cyclooxygenase (COX)–2 or 5-lipoxygenase (5-LO) are upregulated in a number of epithelial tumors, but to date there are hardly any data about the expression of these markers in meningiomas. To find possible targets for chemotherapeutic intervention, the authors evaluated the expression of AA derivatives at different molecular levels in meningiomas. Methods One hundred and twenty-four meningioma surgical specimens and normal human cortical tissue samples were immunohistochemically and cytochemically stained for COX-2, COX-1, 5-LO, and prostaglandin E receptor 4 (PTGER4). In addition, Western blot and polymerase chain reaction (PCR) analyses were performed to detect the presence of eicosanoids in vivo and in vitro. Results Sixty (63%) of 95 benign meningiomas, 21 (88%) of 24 atypical meningiomas, all five malignant meningiomas, and all normal human cortex samples displayed high COX-2 immunoreactivity. All cultured specimens and IOMM-Lee cells stained positive for COX-2, COX-1, 5-LO, and PTGER4. The PCR analysis demonstrated no changes in eicosanoid expression among meningiomas of different World Health Organization grades and in normal human cortical and dura mater tissue. Conclusions Eicosanoid derivatives COX-1, COX-2, 5-LO, and PTGER4 enzymes show a high universal expression in meningiomas but are not upregulated in normal human cortex and dura tissue. This finding of the ubiquitous presence of these enzymes in meningiomas offers an excellent baseline for testing upcoming chemotherapeutic treatments.

Early Colonic Lesions in Experimental Shigella Infection in Rhesus Monkeys: Revisited

1982 ◽  
Vol 19 (7_suppl) ◽  
pp. 1-8 ◽  
Author(s):  
A. Takeuchi
Keyword(s):  
Epithelial Cells ◽  
Lamina Propria ◽  
Macaca Mulatta ◽  
Rhesus Monkeys ◽  
Goblet Cells ◽  
Intestinal Lumen ◽  
Surface Epithelium ◽  
Bacterial Invasion ◽  
Acute Colitis ◽  
Columnar Cells

Rhesus monkeys (Macaca mulatta), given 3 × 108 to 5 × 1010Shigella flexneri 2a orally, developed signs of acute shigellosis within 24 hours. A diffuse acute colitis was well established at 48 hours. The inflammatory reaction was confined to the mucosa. The submucosa showed only edema. The shigellae were found predominantly in the columnar cells of the surface epithelium, less frequently in those of the crypt, and least frequently in the lamina propria. Shigella bacilli invaded the columnar cells from the intestinal lumen. The bacilli multiplied within epithelial cells and spread laterally to adjacent epithelial cells and penetrated the lamina propria. The bacterial invasion affected epithelial cells unevenly and resulted in the disappearance of goblet cells and pyknotic shrinkage of the surface epithelial cells. Epithelial cells had abnormal and accelerated exfoliation which resulted in multifocal epithelial defects. There was a distinct correlation between the quantity of bacilli present in tissues and the intensity of the inflammatory response. The small intestines were spared.

scholarly journals Effects of Nonsteroidal Anti-Inflammatory Drugs onHelicobacter pylori-Infected Gastric Mucosae of Mice: Apoptosis, Cell Proliferation, and Inflammatory Activity

2001 ◽  
Vol 69 (8) ◽  
pp. 5056-5063 ◽  
Author(s):  
Tae Il Kim ◽  
Yong Chan Lee ◽  
Kwang Hyoung Lee ◽  
Jae Ho Han ◽  
Chae Yoon Chon ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Inflammatory Activity ◽  
Prostaglandin E ◽  
Gastric Epithelial Cells ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
H Pylori ◽  
Cox 1

ABSTRACT Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation inH. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E2 levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E2 levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.

Kinetic effect of oestrogen on secretion of prostaglandins E2 and F2α in bovine oviduct epithelial cells

2017 ◽  
Vol 29 (3) ◽  
pp. 482 ◽  
Author(s):  
Zhiheng Dong ◽  
Nan Zhang ◽  
Wei Mao ◽  
Bo Liu ◽  
Na Huang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dynamic Change ◽  
Extracellular Fluid ◽  
Prostaglandin F2α ◽  
Subsequent Decrease ◽  
Polymerase Chain ◽  
Cox 2 ◽  
Oviduct Epithelial Cells ◽  
In Cell Western ◽  
Cox 1

This study aimed to investigate the effect of oestrogen on prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) secretion in bovine oviduct epithelial cells. Bovine oviduct epithelial cells were obtained from the lumen of fresh bovine oviducts. Quantitative real-time polymerase chain reaction and in-cell western assays were used to measure PGE2 and PGF2α synthase activity and enzyme-linked immunosorbent assays were used to detect the concentrations of the two prostaglandins in extracellular fluid. We observed that oestradiol caused a short-term increase in cyclo-oxygenase-2 (COX-2), which stimulated PGE2 and PGF2α secretion, and that a subsequent decrease in COX-2 and an increase in cyclo-oxygenase-1 (COX-1) produced a high PGE2 : PGF2α ratio. These findings reflect the dynamic change in PGE2 and PGF2α levels under the influence of oestrogen, which may be essential for fertilisation.

Adult human colonic subepithelial myofibroblasts express extracellular matrix proteins and cyclooxygenase-1 and -2

1997 ◽  
Vol 273 (6) ◽  
pp. G1341-G1348 ◽  
Author(s):  
Y. R. Mahida ◽  
J. Beltinger ◽  
S. Makh ◽  
M. Göke ◽  
T. Gray ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Function ◽  
Primary Cultures ◽  
Collagen Type Iv ◽  
Prostaglandin E ◽  
Adult Human ◽  
Ecm Proteins ◽  
Cox 1

Interactions between epithelial cells and subepithelial myofibroblasts are increasingly recognized as important in the regulation of epithelial cell function. We have established primary cultures of subepithelial myofibroblasts from adult human colonic mucosal samples denuded of epithelial cells and maintained in culture. During culture of mucosal tissue, subepithelial myofibroblasts migrated out via basement membrane pores before establishment in culture. Despite prolonged culture and passage, the myofibroblasts maintained their phenotype, as demonstrated by expression of α-smooth muscle actin and vimentin. The cells expressed transcripts and protein for cyclooxygenase (COX)-1 and -2 enzymes, and their release of prostaglandin E2(PGE2) was inhibited by selective COX-1 and -2 inhibitors. The myofibroblasts also expressed the extracellular matrix (ECM) proteins collagen type IV, laminin-β1 and -γ1, and fibronectin. Adult human colonic subepithelial myofibroblasts may influence epithelial cell function via products of COX-1 and -2 enzymes, such as PGE2 and secreted ECM proteins.

Differential lamina propria cell migration via basement membrane pores of inflammatory bowel disease mucosa

1998 ◽  
Vol 115 (4) ◽  
pp. 841-848 ◽  
Author(s):  
Mark E. McAlindon ◽  
Trevor Gray ◽  
Alison Galvin ◽  
Herbert F. Sewell ◽  
Daniel K. Podolsky ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cell Migration ◽  
Basement Membrane ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Membrane Pores ◽  
Inflammatory Bowel

scholarly journals Pulmonary and Cardiorenal Cyclooxygenase-1 (COX-1), -2 (COX-2), and Microsomal Prostaglandin E Synthase-1 (mPGES-1) and -2 (mPGES-2) Expression in a Hypertension Model

2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Zaher A. Radi ◽  
Robert Ostroski
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Cellular Localization ◽  
Vascular Endothelial Cells ◽  
Prostaglandin E ◽  
Human Hypertension ◽  
Collecting Ducts ◽  
Cox 2 ◽  
Convoluted Tubules ◽  
Cox 1

Hypertensive mice that express the human renin and angiotensinogen genes are used as a model for human hypertension because they develop hypertension secondary to increased renin-angiotensin system activity. Our study investigated the cellular localization and distribution of COX-1, COX-2, mPGES-1, and mPGES-2 in organ tissues from a mouse model of human hypertension. Male (n=15) and female (n=15) double transgenic mice (h-Ang 204/1 h-Ren 9) were used in the study. Lung, kidney, and heart tissues were obtained from mice at necropsy and fixed in 10%neutral buffered formalin followed by embedding in paraffin wax. Cut sections were stained immunohistochemically with antibodies to COX-1, COX-2, mPGES-1, and mPGES-2 and analyzed by light microscopy. Renal expression of COX-1 was the highest in the distal convoluted tubules, cortical collecting ducts, and medullary collecting ducts; while proximal convoluted tubules lacked COX-1 expression. Bronchial and bronchiolar epithelial cells, alveolar macrophages, and cardiac vascular endothelial cells also had strong COX-1 expression, with other renal, pulmonary, or cardiac microanatomic locations having mild-to-moderate expression. mPGES-2 expression was strong in the bronchial and bronchiolar epithelial cells, mild to moderate in various renal microanatomic locations, and absent in cardiac tissues. COX-2 expression was strong in the proximal and distal convoluted tubules, alveolar macrophages, and bronchial and bronchiolar epithelial cells. Marked mPGES-1 was present only in bronchial and bronchiolar epithelial cells; while mild-to-moderate expression was present in other pulmonary, renal, or cardiac microanatomic locations. Expression of these molecules was similar between males and females. Our work suggests that in hypertensive mice, there are (a) significant microanatomic variations in the pulmonary, renal, and cardiac distribution and cellular localization of COX-1, COX-2, mPGES-1, and mPGES-2, and (b) no differences in expression between genders.

Expression of Apoptotic Epithelial Cells Within Lamina Propria Beneath the Basement Membrane Triggers Dextran Sulfate Sodium-Induced Colitis

2008 ◽  
Vol 53 (9) ◽  
pp. 2443-2451 ◽  
Author(s):  
Kazuko Shichijo ◽  
Makoto Ihara ◽  
Mohammed Shawkat Razzaque ◽  
Mutsumi Matsuu-Matsuyama ◽  
Toshiyuki Nakayama ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Basement Membrane ◽  
Lamina Propria ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

scholarly journals Evaluation of TGF-β1 and EGFR in Cleft Affected Lip Mucosa

2021 ◽  
Vol 28 (1) ◽  
pp. 14
Author(s):  
Olga Rimdenoka ◽  
Māra Pilmane
Keyword(s):  
Epithelial Cells ◽  
Lamina Propria ◽  
Oral Mucosa ◽  
Rank Correlation ◽  
Control Group ◽  
Orofacial Cleft ◽  
Tissue Samples ◽  
Moderate Number ◽  
Healthy Mucosa ◽  
Tgf Β1

Background. The morphopathogenesis of orofacial cleft development is only partly understood; therefore, it is important to identify factors, which possibly could be involved in it. The aim of the study was to evaluate the distribution of TGF-β1 and EGFR-containing cells in cleft affected lip mucosa.Materials and Methods. The study group included lip mucosa tissue samples from 14 patients with orofacial cleft. The control group contained 11 healthy oral mucosa tissue samples. The tissue sections were stained by immunohistochemistry for TGF-β1 and EGFR. The expression of positive structures was graded semiquantitatively. IBM SPSS 26.0 was used for statistical analysis, Spearman`s rank correlation and Mann-Whitney U tests were performed.Results. Mostly few to moderate number (+/++) of TGF-β1-containing cells was found in epithelium, also the same number of fibroblasts and macrophages was seen in the lamina propria of cleft affected lip mucosa. Meanwhile, healthy oral mucosa on average demonstrated a moderate number (++) of TGF-β1-containing epithelial cells, fibroblasts, and macrophages. A variable, mostly indistinct number of EGFR-containing cells was seen in the epithelium of cleft affected lip mucosa, meanwhile, mostly no (0) EGFR positive cells were found in the epithelium of healthy mucosa. Statistically significantly less TGF-β1-containing cells were found in the epithelium of cleft affected lip mucosa than in the healthy mucosa (U=33.000; p=0.015). Also, the lamina propria of cleft affected lip mucosa showed statistically significantly less TGF-β1 immunoreactive fibroblasts and macrophages than the healthy mucosa (U=28.500; p=0.006).Conclusions. The decreased number of TGF-β1-containing epithelial cells, fibroblasts and macrophages in cleft affected lip mucosa proves the role of problematic tissue remodelation in the cleft pathogenesis. The distribution of EGFR in cleft affected and healthy mucosa is similar and possibly does not play a role in the cleft development of humans.

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