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PubMed1999

Benign and malignant serous and endometrioid epithelium in the omentum.

OBJECTIVES: Benign and malignant serous and endometrioid epithelial proliferations are found in the omentum, where their presence may be interpreted either as metastases from Müllerian tumors elsewhere or as primary peritoneal tumors. The present study was undertaken in an attempt to gather data that might help resolve the issue. METHODS: The ratios of serous epithelium to endometrioid epithelium in the omentum, in both the benign and malignant states, were determined for cases from January 1985 to July 1997 and January 1991 to December 1997, respectively. RESULTS: In ovarian carcinoma, the ratio of malignant serous epithelium to endometrioid epithelium involving the omentum is 15:1. This is comparable to the ratio of benign serous epithelium to endometrioid epithelium in the omentum, which is 10:1. The ratio of primary peritoneal serous carcinoma to endometrioid carcinoma is 10.5:1. CONCLUSION: It seems not reasonable that endometrioid carcinoma of the ovary is 15 times less likely to metastasize to the omentum than its serous counterpart. The ratio, however, is not unreasonable if endometrioid and serous carcinomas arise from preexisting endometrioid or serous epithelium. We conclude that serous and endometrioid carcinomas may arise primarily in the omentum and, in at least some cases, may derive from their benign counterparts.

Endometriosis↗
PubMed1982

Culturing of renal collecting duct epithelium as globular bodies.

Thin kidney cortex explants from newborn rabbits, consisting of the capsula fibrosa with an adherent layer of nephrogenic material (s-shaped bodies and collecting duct anlagen) were isolated and cultured for various periods (up to 15 days) by conventional procedures. Within the first 24 h of culturing, it was observed that the explants form globular bodies covered by a monolayer epithelium. The cells are cuboidal or cylindrical, and may, in later stages, consist of two or even more cell layers. The epithelium shows a polar differentiation, with deep tight junctions at the apical poles and lateral intercellular spaces opening to the basal surface. A basal lamina is not consistently developed. The support of the epithelium consists of fibroblasts and degenerating tissue elements of the explants. It can be shown that the epithelium is derived from the anlagen of the collecting ducts. Structurally, the epithelium resembles a collecting duct epithelium. The experimental system is considered as a useful model to study metabolism and function of the renal collecting duct epithelium, as well as developmental problems, such as cell migration, outgrowth, and differentiation.

Animals↗
PubMed1987

Endocrine cells in ectocervical epithelium. An immunohistochemical and ultrastructural analysis.

A systematic study of endocrine cells in the ectocervix was carried out using histochemical, immunohistochemical and ultrastructural techniques. Serotonin and calcitonin immunoreactive cells were demonstrated in this site. Serotonin and calcitonin immunoreactivities were coexpressed in the same endocrine cell. These distinctive cells were encountered in two main morphological varieties of ectocervical epithelium. Normal-appearing stratified squamous epithelium contained only very rare serotonin and calcitonin cells. In contrast, endocrine cells were fairly abundant in a specific epithelium termed "transitional-like". This type of epithelium was not only confined to the transformation zone but could also extend onto the portio as far as the vaginal cut margin. In some cases, transitional-like epithelium bore morphological resemblance to urothelium. In other cases, it could be regarded as basal cell hyperplasia or immature squamous metaplasia. Of interest, serotonin and calcitonin cells have been well-documented as normal inhabitants of some other non-squamous epithelia, such as urothelium or pseudostratified columnar epithelium. Therefore, it is suggested that certain ectocervical epithelia show some similarities to urothelium, in respect of their morphological appearance and endocrine profile. Further investigations using more objective and specific markers of urothelial cells are needed to assess the exact degree of homology connecting all these types of epithelium.

Calcitonin↗
PubMed2007

Antimicrobial peptide modulation in a differentiated reconstructed gingival epithelium.

Gingival innate immunity has been studied by using biopsies and normal or transformed epithelial cell monolayers. To overcome individual biological variabilities and as a physiological alternative, we have proposed using a reconstructed tissue equivalent. In this study, we investigated the functionality and the stage of differentiation of a reconstructed human gingival epithelium. We also characterized this epithelium at the molecular level to investigate its differentiation stage compared with native human gingival epithelium. The expression levels and localization of markers related to proteins and lipids of well-differentiated stratified epithelium, such as cytokeratins, cornified envelope proteins and enzymes, or to factors in lipid synthesis and trafficking were examined. Immunohistochemistry revealed similar localization patterns in both types of epithelia and mRNA quantification showed a close resemblance of their expression profiles. We further revealed that, like native gingiva, reconstructed gingival epithelium was able to respond to pro-inflammatory or lipopolysaccharide stimuli by producing antimicrobial peptides hbetaD-2, hbetaD-3 or LL-37. Finally, we demonstrated that reconstructed human gingival epithelium, as a model, was good enough to be proposed as a functional equivalent for native human gingival epithelium in order to study the regulation of gingival innate immunity against periodontal infections.

Antimicrobial Cationic Peptides↗
PubMed1996

Ultrastructural evidence for transepithelial calcium transport in the anterior sternal epithelium of the terrestrial isopod Porcellio scaber (Crustacea) during the formation and resorption of CaCO3 deposits

Before the molt, terrestrial isopods store large amounts of calcium carbonate between the epithelium and the old cuticle of the first four anterior sternites. In order to test whether the anterior sternal epithelium has specific structural differentiations indicative of transepithelial ion transport, the anterior sternal epithelium and, as a control, the posterior sternal epithelium were studied using electron-microscopical techniques. During the formation of calcium carbonate deposits, the basolateral plasma membrane of the anterior sternal epithelium forms an elaborate interconnected network of interstitial dilations and channels. Numerous osmiophilic granules occur within this basolateral intercellular network during resorption of the calcium carbonate deposits. Electron energy-loss spectroscopy of the osmiophilic granules indicates that they contain calcium. During the resorption of the calcium carbonate deposits, the apical plasma membrane of the anterior sternal epithelium has many subcuticular folds. An interstitial network, osmiophilic granules, and apical, subcuticular folds do not occur in the posterior sternal epithelium. Taken together, these structural features are indicative of transepithelial ion transport and are probably necessary for the formation and resorption of the anterior sternal calcium carbonate deposits.

Journal Article↗
PubMed1990

Epithelium-derived inhibitory factor in human bronchus.

The potencies of histamine and methacholine were significantly increased by approximately 2- and 5-fold respectively in human non-diseased isolated bronchi on removal of the epithelium. In contrast, no increases in spasmogen potency were observed following epithelium removal in bronchi obtained from a sample of asthmatic human lung. The failure of epithelium removal to increase asthmatic bronchial sensitivity to histamine may have been due to a reduction in the release of an epithelium-derived inhibitory factor (EpDIF) resulting from disease-induced epithelial damage. A co-axial bioassay system in which endothelium-denuded rat aorta was used as the assay tissue was used to detect the release of a vasorelaxant EpDIF from human bronchial tissue. Histamine (100 microM) and methacholine (25 microM), in the presence of indomethacin (5 microM), reduced phenylephrine-induced tone in endothelium-denuded rat aorta in co-axial assemblies by 75 +/- 11 and 67 +/- 9% respectively. Removal of the bronchial epithelium abolished these responses, indicating that they were mediated by an EpDIF. It is possible that human airway smooth muscle is sensitive to this vasorelaxant EpDIF and that the absence of the source of this factor following epithelium removal caused the increases in sensitivity to spasmogens. Alternatively, the human bronchial epithelium may also release an EpDIF selective for airway smooth muscle.

Animals↗
PubMed1984

3T3-L1 adipocytes promote the growth of mammary epithelium.

Murine mammary epithelium grows in association with predominantly adipocyte stroma in vivo. To investigate potential growth-promoting effects of adipocytes on mammary epithelium, we developed a co-culture system of mammary epithelium and adipocytes by taking advantage of the 3T3-L1 cell line. These cells undergo adipocyte differentiation when the culture reaches confluence and growth ceases. Mid-pregnant murine mammary epithelium was plated on lethally irradiated feeder layers of 3T3-L1 adipocytes, undifferentiated 3T3-L1 cells, 3T3-C2 fibroblasts (a subclone of 3T3 cells that does not undergo adipocyte differentiation), or tissue culture plastic. Mammary epithelial colony size on adipocyte feeder layers was 2-fold larger than colonies on 3T3-C2 cells and 4-fold larger than colonies on tissue culture plastic. Measurement of tritiated thymidine [3H]TdR incorporation and labelling index in mammary cells was significantly higher on adipocytes than on other feeder layers or plastic. There was a 6-fold increase in mammary cell number after 5 days in culture when mammary epithelium was plated on substrate-attached material ('extracellular matrix') derived from 3T3-L1 cells and a 4-fold increase in cell number when plated on plastic in conditioned medium derived from 3T3-L1 adipocytes compared with growth on plastic in unconditioned medium. We conclude that interaction of mammary epithelium with adipocytes results in a marked increase in proliferation of mammary epithelium and that extracellular components may mediate this effect.

Adipose Tissue↗
PubMed2004

Comparison of morphological and functional characteristics of primary-cultured human conjunctival epithelium and of Wong-Kilbourne derivative of Chang conjunctival cell line.

PURPOSE: To analyze the relevance of a human conjunctival cell line in a study of conjunctival epithelium. We investigated and compared the effects of IFNgamma and TNFalpha in a primary culture of human conjunctiva and in a human conjunctival cell line. METHODS: A primary-cultured human conjunctival epithelium and a human conjunctival cell line (Chang cells) were treated for 72 hr with 20, 200, 400 and 600 U ml(-1) IFNgamma or with 1100 and 11,000 U ml(-1) TNFalpha. Then, the expression of HLA DR, CD40, CD44, CD63, CD80, CD86, Fas receptor, E-cadherin, ICAM-1, MUC1, cytokeratins and vimentin were investigated by flow cytometry. Cell morphology was studied with phalloidin staining. Apoptosis was detected by flow cytometry with Annexin V and via cell cycle analysis. RESULTS: The primary culture of human conjunctival epithelium expressed cytokeratin K4, non-keratinized squamous epithelial marker. Chang cells presented a more dedifferentiated phenotype and were cytokeratin K4 negative. In primary-cultured cells, IFNgamma (600 U ml(-1)) induced only a low level of apoptosis and a significant upregulation of most tested proteins such as HLA DR, Fas, ICAM-1, CD40 and CD63. In the Chang cell line, IFNgamma induced a significant level of apoptosis at concentrations of 200, 400 and 600 U ml(-1). HLA DR and CD63 were induced at lower levels than in primary-cultured cells. Other proteins were modified in a similar manner after IFNgamma treatment in both systems. In the primary-cultured cells, TNFalpha induced an important upregulation of ICAM-1, Fas and CD40 whereas CD44 and CD63 were significantly decreased. Conversely, only a very weak alteration of CD63 and ICAM-1 was observed in the Chang cell line after TNFalpha treatment. CONCLUSIONS: A primary culture of a human conjunctival epithelium demonstrated well-defined epithelial features. TNFalpha and IFNgamma, two inflammatory cytokines, induced different effects in both cellular systems, in a primary-cultured conjunctival epithelium and a human conjunctival cell line. Inflammation-related molecules were highly upregulated in the primary culture and, to a lesser extent, in the Chang cell line. Thus, the Chang cell line differs in certain features from a primary culture of human conjunctival epithelium, a fact which emphasizes the complexity of interpretation of in vitro data and this should be taken into consideration in in vitro studies of human conjunctival epithelium.

Antigens, Surface↗
PubMed2005

Integrity of airway epithelium is essential against obliterative airway disease in transplanted rat tracheas.

BACKGROUND: The pathogenesis of obliterative bronchiolitis after lung transplantation requires further elucidation. In this study we used rat trachea transplantation to examine the role of epithelium in the progression of obliterative airway disease. METHODS: Normal and denuded (i.e., epithelium removed) trachea grafts from Lewis (LEW) and Brown Norway (BN) rats were transplanted sub-cutaneously into LEW rats. Viable trachea epithelial cells (to recover epithelium) were seeded into the lumen of some of the denuded tracheas. Grafts were removed at different time-points between 2 days and 8 weeks after transplantation. Histologic analysis was performed to evaluate cellular infiltration of inflammatory cells, loss of epithelium, and obliteration of trachea lumen. RESULTS: Obliteration was found to occur in trachea transplants after loss of epithelium, caused by rejection in allografts or by enzymatic denudation in isografts. In these situations, fibroblasts started to proliferate and migrate into the lumen in the second week after transplantation. Obliteration could be prevented when epithelial integrity was restored by seeding epithelial cells; no obliteration occurred when denuded trachea isografts were seeded with epithelial cells, whereas non-seeded denuded tracheas were obliterated at Day 6 after transplantation. CONCLUSIONS: We conclude that integrity of airway epithelium is essential for rat trachea transplants to be safeguarded from obliterative airway disease. For clinical lung transplantation the results of our study suggest that protection of the integrity of airway epithelium may be important in preventing the development of obliterative bronchiolitis.

Animals↗
PubMed2004

Evaluation of different toxicity assays applied to proliferating cells and to stratified epithelium in relation to permeability enhancement with glycocholate.

The purpose of the present study was to evaluate different toxicity assays for use on proliferating buccal TR146 cells and on stratified TR146 epithelium and to compare these results to the permeability enhancing effect of glycocholate (GC). Both the proliferating cells and the epithelium were exposed to different GC concentrations for 4 h. The MTS/PMS assay and neutral red (NR) retention were performed along with quantitation of ATP, lactate dehydrogenase (LDH) and extracellular protein. The toxicity was calculated as the IC50 value relative to the control. Increase in 3H-mannitol permeability across the epithelium concurrent with a decrease in the transepithelial electrical resistance (TEER) was also determined. The robustness of the epithelium was significantly higher than that of the proliferating cells (P <0.01). The ATP assay was the most sensitive assay with IC50 values of 6.4 and 11.5 mM for proliferating cells and epithelium, respectively. Intracellular LDH quantitation was the least sensitive method and extracellular LDH could not be used as a measure of toxicity partly due to interaction between LDH and GC. The effect on permeability and TEER could be correlated to the IC50 values obtained for the epithelium. The present study clearly demonstrates that for a correlation between toxicity and permeability enhancement, both studies should be performed on the epithelium.

Adenosine Triphosphate↗
PubMed2000

Thapsigargin, a Ca(2+)-ATPase inhibitor, relaxes guinea pig tracheal smooth muscle by producing epithelium-dependent relaxing factors.

A non-phorbol ester-type tumor promoter, thapsigargin has been reported to deplete Ca(2+) stores in endothelial cells by inhibiting Ca(2+)-ATPase, which in turn increases intracellular Ca(2+) by mobilization of extracellular Ca(2+), leading to activation of constitutive nitric oxide synthase (cNOS) and resultant generation of nitric oxide (NO). In the present study, to evaluate the role of Ca(2+) in the release of epithelium-dependent relaxing factor (EpDRF), we determined the effect of thapsigargin (10(-6) M) on the contraction evoked by exogenous Ca(2+) or acetylcholine (10(-5) M) in epithelium-denuded or epithelium-intact smooth muscle from guinea pig trachea. The following results were obtained: (1) In epithelium-denuded smooth muscle, the contraction evoked by exogenous Ca(2+) in Ca(2+)-free solution or by acetylcholine (10(-5) M) in Ca(2+)-containing solution did not change within 20 min after thapsigargin application, but the contraction evoked by exogenous Ca(2+) increased markedly after 120 min, indicating that thapsigargin had no effect on smooth muscle itself within 20 min of application. The following experiments were performed within 20 min of thapsigargin application. (2) In epithelium-intact smooth muscle, thapsigargin significantly suppressed the contraction evoked by acetylcholine, suggesting that thapsigargin stimulate the epithelium to produce EpDRF. N(G)-nitro-L-arginine methylester (L-NAME) partly, but significantly, attenuated this inhibitory effect of thapsigargin. (3) In epithelium-denuded smooth muscle, atropine (10(-6) M) and L-NAME (10(-5) M) did not change the contraction evoked by exogenous Ca(2+) after application of thapsigargin, suggesting that thapsigargin did not stimulate acetylcholine and NO release from nerve terminals. These results suggest that thapsigargin (10(-6) M) may stimulate EpDRF, including NO and other factor(s) by Ca(2+)-dependent mechanisms.

Acetylcholine↗
PubMed1991

The potential role of the ovine pharyngeal tonsil in respiratory tract immunity: a scanning and transmission electron microscopy study of its epithelium.

The mucosal epithelium of the pharyngeal tonsil was studied in 10 conventionally raised sheep by scanning and transmission electron microscopy. The surface of the tonsil was covered by two types of topographically and ultrastructurally distinct epithelium. The epithelium overlying the lymphoid follicle region (follicle-associated epithelium) was compressed by adjacent ciliated epithelium and consisted of predominantly non-ciliated cells of varying height. The majority of these cells possessed microvilli or microfolds of varying number, height and density on their surface. Small numbers of squamous cells and, occasionally, intermediate cells were also present in these areas. Ultrastructurally, the microvillous cells showed features similar to M cells which occur in other mucosal sites. They contained cytoplasmic vesicles and vacuoles and formed intercellular digital junctions. Between these cells was a heavy infiltration of lymphoid cells. Focal disintegration of the mucosal epithelium was occasionally seen. The epithelium covering non-follicle areas consisted of mainly ciliated cells interspersed with some goblet cells and squamous cells, morphologically resembling those elsewhere in the respiratory tract. These findings have provided evidence which confirms that the ovine pharyngeal tonsil is part of the respiratory tract-associated lymphoid tissue.

Animals↗
PubMed1997

Mitogenic responses of rat nasal epithelium to hexamethylphosphoramide inhalation exposure.

Hexamethylphosphoramide (HMPA) is a rat nasal carcinogen that induces squamous cell carcinomas in the anterior portions of the nasal cavity following chronic inhalation exposures as low as 50 ppb. These tumors may arise as a result of P-450-mediated release of formaldehyde (HCHO), a known rat nasal carcinogen. The goal of this research was to investigate early responses of the nasal epithelium to inhaled HMPA. Rats were exposed nose-only to approximately 3 ppm HMPA for 6 h, and killed 18, 48, 96 or 144 h post-exposure. In a separate study, rats were exposed nose-only for 6 h for 1, 2, 3, or 5 consecutive days and killed 18 or 96 h post-exposure. With both single and repeated doses of HMPA, there was no evidence of cytotoxicity in the anterior nose. Olfactory degeneration and necrosis of the dorsal meatus, Bowman's glands and tips of the ethmoid turbinates increased in severity with repeated exposures to HMPA. Cell proliferation was assessed in levels of nasal tissue that included regions of squamous, respiratory, transitional and olfactory epithelium. Regional induction of cell proliferation was measured by BrdU incorporation, and reported as the number of labeled cells/mm basement membrane. At 18 h after a single exposure, there was an increase in cell proliferation in squamous epithelium, which returned to control levels within 48 h. A transitory increase in cell proliferation was observed regions of respiratory and transitional epithelium, although the response of each tissue, in terms of magnitude and peak time of response post-exposure, also differed. Along the dorsal meatus in Level 9, olfactory labeling initially decreased, returned to control levels by 96 h, but again declined at 144 h post-exposure. In repeat dose studies, the squamous epithelium response was variable 18 h post-exposure. For respiratory and transitional epithelium, increased cell proliferation 18 h post-exposure was correlated with increased dose (exposure) of HMPA. Cell proliferation responses following two or more exposures returned to near control levels within 96 h post-exposure. In conclusion, HMPA induced cell proliferation, but not cytotoxicity, in the anterior nose at approximately 3 ppm. These data suggest that HMPA induces proliferative, perhaps mitogenic, responses in the nasal epithelium, and this response may facilitate the fixation of low level genetic damage induced by liberated HCHO.

Administration, Inhalation↗
PubMed2002

Viability of cultured periodontal pocket epithelium cells and Porphyromonas gingivalis association.

OBJECTIVES: Porphyromonas gingivalis, one of the key pathogens in the development of periodontitis, produces a number of virulence factors that might explain its pathogenicity. One of them is the ability to adhere and invade pocket epithelium. The aim of this study was to follow, over time, the association of P. gingivalis and consequent morphological changes of the pocket epithelium cells. MATERIAL AND METHODS: The association capacity of four P. gingivalis serotypes [K1, K2, K4, K- (nonencapsulated)] with in vitro cultured mono-layers from periodontal pocket epithelial cells of patients with periodontitis, was followed by fluorescence microscopy and bacterial culture. The contact time between bacteria and epithelium cells ranged from 45 min to 8 h. The microscopic evaluation allowed differentiation between dead and living cells (bacteria as well as epithelium) and description of the morphological changes after association. RESULTS: A highly significant difference in the number of associating bacteria was found between dead and living epithelium cells, and between non-capsulated and capsulated strains. A significant increase in the proportion of dead pocket epithelium cells was found with prolonged association time. The morphological changes (rounding of the epithelial cell, detachment from the glass cover-slip and loss of intercellular contact) occurred faster for mono-layers inoculated with the non-encapsulated P. gingivalis strain. CONCLUSIONS: This study indicates that dead pocket epithelium cells harbor more P. gingivalis cells, and that a positive correlation exists between contact time and cell death. For the P. ginigvalis species, non-encapsulated strains associate in higher number. As a result, the damage they cause to the host cell seems to occur faster than occurs in encapsulated strains. As such, cell death can be seen as the end-result of bacterial association.

Bacterial Adhesion↗
PubMed2002

Merkel-like cells in Malassez epithelium in the periodontal ligament of cats: an immunohistochemical, confocal-laser scanning and immuno electron-microscopic investigation.

The cellular heterogeneity of Malassez epithelium (ME) residing in the periodontal ligament has recently been reported, and the presence and coexistence of the neuropeptides calcitonin gene-related peptide (CGRP), substance P (SP) and vasoactive intestinal peptide (VIP) in single cells in ME has been shown (1). However, the identity of these neuroendocrine cells has so far not been verified. This study was undertaken in order to elucidate the identity of the neuroendocrine cells in ME by means of transmission electron microscopy, confocal scanning microscopy and immunohistochemistry using antibodies to protein gene product (PGP) 9.5 and cytokeratin 20 (CK). Gingival tissue was included in the study as a positive control for identification of Merkel-like cells in oral epithelium. CK 20 immunopositive cells were present in both Malassez epithelium and in basal cell layers of gingival epithelium showing a distribution consistent with PGP 9.5 labelled cells in both epithelia. The results from PGP 9.5 immuno electron microscopy clearly evidenced the presence of single, intensely labelled cells and some nerve fibres invested between the Malassez epithelial cells. The conformity of the immunopositive cells in Malassez and gingival epithelium verified by double immunolabelling with PGP 9.5 and CK 20, indicates that the labelled neuroendocrine cells are identical in ME and in gingival epithelium. This demonstrates that Malassez epithelium not only exhibits neuroendocrine cells, but additionally that the neuroendocrine cells represent Merkel-like cells.

Animals↗
PubMed2003

The airway epithelium: structural and functional properties in health and disease.

The major function of the respiratory epithelium was once thought to be that of a physical barrier. However, it constitutes the interface between the internal milieu and the external environment as well as being a primary target for inhaled respiratory drugs. It also responds to changes in the external environment by secreting a large number of molecules and mediators that signal to cells of the immune system and underlying mesenchyme. Thus, the epithelium is in a unique position to translate gene-environment interactions. Normally, the epithelium has a tremendous capacity to repair itself following injury. However, evidence is rapidly accumulating to show that the airway epithelium of asthmatics is abnormal and has increased susceptibility to injury compared to normal epithelium. Areas of detachment and fragility are a characteristic feature not observed in other inflammatory diseases such as COPD. In addition to being more susceptible to damage, normal repair processes are also compromised. Failure of appropriate growth and differentiation of airway epithelial cells will cause persistent mucosal injury. The response to traditional therapy such as glucocorticoids may also be compromised. However, whether the differences observed in asthmatic epithelium are a cause of or secondary to the development of the disease remains unanswered. Strategies to address this question include careful examination of the ontogeny of the disease in children and use of gene array technology should provide some important answers, as well as allow a better understanding of the critical role that the epithelium plays under normal conditions and in diseases such as asthma.

Asthma↗
PubMed2006

Identification of mouse genes with highly specific expression patterns in differentiated intestinal epithelium.

BACKGROUND & AIMS: Few genes that regulate intestinal epithelium development, homeostasis, or function are known. We reasoned that potential candidate regulators of these processes could be identified based on their activation during intestinal epithelium development and their subsequent specific and restricted expression. METHODS: Genes were identified by differential display and microarray analyses, further selected according to sequence and UniGene expression profiles, and analyzed by RNA in situ hybridization of mouse fetal and adult intestines and in intestinal polyp tissue. RESULTS: Five genes with unknown physiological function predominantly or exclusively expressed in the intestinal epithelium were identified. Their expression is activated at distinct times during intestinal development and maturation and is maintained in highly specific, spatially distinct patterns in the adult intestinal epithelium. Two of the genes were up-regulated in intestinal tumors, 1 was down-regulated, and 2 were apparently unaltered. CONCLUSIONS: Based on sequence and expression, the identified genes represent good candidates for regulators of intestinal epithelium integrity or function. Their expression patterns suggest a morphologically not obvious molecular regionalization of the intestinal epithelium along the crypt villus axis. This approach should be an efficient means to identify novel genes required for intestinal epithelium homeostasis and function.

Animals↗
PubMed1999

Airway responsiveness: role of inflammation, epithelium damage and smooth muscle tension.

The purpose of this study was the effect of epithelium damage on mechanical responses of airway smooth muscles under different resting tension. We performed acetylcholine (ACh) (10(-5) M)-induced contraction on tracheal strips from 30 rabbits in five groups (0.5, 1, 1.5, 2 and 2.5 g) before and after epithelium removal. At low resting tension (0.5-1.5 g), the epithelium removal decreased the ACh-induced contractions. At 2 g resting tension, the epithelium removal increased the ACh-induced contractions of airways with intact epithelium about 20%. At 2.5 g resting tension, the elevation of contraction is about 25% (P<0.01). Consequently, after epithelium loss, the resting tension determines the airway smooth muscles responsiveness. In asthma, mediators such as ACh act on already contracted inflammatory airways, which results in additional increase of contraction. In contrast, low resting tension, a condition that simulates normal tidal breathing, protects from bronchoconstriction even when the epithelium is damaged.

Acetylcholine↗