Exfoliated epithelial cells are in a situation similar to freshly isolated primary cells. Primary cells are inoculated as single-cell suspensions or small clumps of cellular aggregates. These cells have also lost contact with the tissue architecture companion fibroblasts, epithelial cell neighbors, and with the extracellular matrix , as well as with the nervous regulation or the blood nutriments.
So even if some cells are exfoliated in a nutritious matrix milk for instance , they may have to trigger a survival mechanism.
Some set of genes are progressively turned-down like clock genes [ 51 ], but in this particular situation, they can be reinduced under specific stimulation in culture. Over the years, the conditions of culture have been adapted to mimic the tissue architecture by creating three-dimensional 3D environment. Recent works have shown that autophagy can be observed during lumen formation in 3D cell cultures in vitro. The MCFA cells are a nontransformed human mammary epithelial cell line, which can form spherical structures called acini in which a layer of polarized epithelial cells surrounds a hollow lumen, mimicking the glandular epithelium in vivo [ 8 , 9 ].
The lesson we can learn from this 3D reconstruction of mammary gland is that epithelial cells are able to flexibly leave or reenter an epithelium. The property is useful for tissular growth as well as to heal rapidly microlesion in the epithelium cell lining. Epithelial cells exfoliated in milk are able to withstand lumen environment. Their biochemical state should be close to the state of cells having lost contact with the 3D reconstructed gland.
In the next section, we present recent works in laboratory rodents which have shown that this capacity of an epithelial cell to adapt to changing environmental conditions is highly context dependent. Laboratory rodent models have been developed to study the inducing effect of nutrient intake on the exfoliation of epithelial cells in the digestive lumen.
On adult rats fastened for 24 hours and refed for one hour, the feeding intake induces exfoliation of quiescent parietal cells at the top of the gastric gland through an unknown exfoliation factor [ 5 ]. Under these conditions, stem cells located in the neck region of gastric glands are believed to be recruited actively to repopulate the surface of the adult rat stomach. On lactating rat pups, we obtained similar results by fastening the pups for 5 hours and allowed them to be reunited with their mother for one hour before sacrifice [ 43 ].
By contrast, on adult laboratory mice, fatty acids like palmitate are inducers of intectin, a protein implicated in the exfoliation of apoptotic cells at the top of the villus of the small intestine within an hour after meal [ 3 ]. These models of nutritional manipulations to induce exfoliation on small intestine of mice [ 3 ] or gastric mucosa of rats [ 5 ] indicate that the mechanism of exfoliation is highly context dependent, but they also open the possibility to develop in vivo studies of anoikis and autophagy in relation with the functioning of peripheral circadian clocks.
The disponibility of laboratory rodent models is of paramount importance to develop in vivo studies on anoikis and its connection with molecular circadian clocks to evaluate the stability of chronobiological molecular information in exfoliated cells.
The proof that exfoliation of quiescent cells is following a circadian rhythm is still missing, probably because the set of physiological parameters leading to the induction of active exfoliation is difficult to handle and the interpretation of data obtained from manual exfoliation is also highly context-sensitive.
In conclusion, exfoliation is a broad term recovering many different biological or experimental situations but as illustrated by the next section, progress in the understanding of the delicate balance between autophagy and apoptosis will help scientists to design new bioassays tailored for specific clinical situations.
Exfoliated cancerous cells of epithelial origin have been the first to be used to help design noninvasive screening assay of cancerous patients [ 52 , 53 ]. The relatively high loss of cancerous epithelial cells by patients as well as the stability of molecular information genetic alterations related to colon cancer, for instance have helped to establish the methodology.
Recently, Chapkin et al. The weak point of this approach is that the morphological information of the cell population is lost during the extraction process of mRNA, and there is no possibility to check for the exact cellular origin of these molecules.
Exfoliation in stools is still highly debated; some visual proof of typical intestinal cells have been published [ 4 , 48 ], but in my experience if whole crypt material or typical colonocytes can be found, most of the time the criticism of Loktionov [ 29 ] that these cells cannot be distinguished from epithelial cells of the anal zone is correct.
The proof of similarity between exfoliated epithelial cells with the ones remaining in the mucosa will be probably easier to perform on gastric epithelium following the seminal work of Aoyama et al.
However, the detection of proteins and structural elements will remain possible only in a limited number of clinical situations narrowing the possibility of using exfoliated epithelial cells as indicator of good health.
Most biological information is highly labile and is rapidly lost after exfoliation. However, a better understanding of the key factors allowing the cellular survival outside the tissue architecture will open new avenues to derive useful screening assays from clinical material.
The detachment of epithelial cells from the tissue architecture triggers both pro- and antiapoptotic signals, such as nuclear factor kappa-B and inhibitor of apoptosis protein family members; these antiapoptotic mechanisms presumably delay the onset of apoptosis and allow cells to survive [ 54 — 56 ].
The balance between these signals and the duration of detachment determine further fate of these cells. Antiapoptotic signals presumably delay the onset of anoikis, allowing cells to survive provided that they can reestablish extracellular matrix contact in a timely manner [ 16 ].
In cells having lost contact with tissular structure, autophagy corresponds to the recycling of cellular material as well as to the cell capacity to mobilize reserves during periods of starvation. Autophagy is a biochemical pathway allowing survival during fasting period which can be stopped at the organism level to prevent self-digestion. There are three main forms of autophagy: microautophagy, macroautophagy, and chaperone-mediated autophagy [ 57 — 59 ].
In macroautophagy, a portion of the cytosol or organelles are sequestered in a double-membrane-bound vesicle, the autophagosome Figures 2 a and 2 b. A core molecule in autophagy regulation is the kinase mammalian target of rapamycin mTOR. By sensing signals that monitor nutrient levels, mTOR can trigger protein translation by specific phosphorylation of the ribosomal protein S6 kinase pS6K [ 60 ].
Recent works on the molecular pathway regulating microtubule-associated protein light chain 3b LC3b and autophagy [ 38 ] support the idea that regulation of autophagy is interconnected with regulation of apoptosis. LC3b may regulate the extrinsic apoptosis pathway in the lung through direct interactions with caveolin-1 and Fas [ 61 ]. Implication of Beclin-2 modifying factor and the antiapoptotic proteins of the Bcl-2 family in the anoikis process have been proposed to play a central role in the survival of human intestinal epithelial cells [ 62 ]; this work partly explains, at the molecular level, the low survival rate of exfoliated epithelial intestinal cells.
However, autophagy has been demonstrated to occur in vivo in the surface epithelial cells of neonatal small intestine of piglets [ 63 ]. In contrast with the data of Hausmann et al. From a physiological point of view in infants as well as in adults, some epithelial cells may survive in a state of macroautophagy close to the surface of the epithelium up to finding their way back in the cellular lining.
A device can then easily remove such cells i. In theory, the physiological status and the genetic profile of these epithelial cells should be close to the ones at the surface of the mucosa. Autophagy can be described in amino-acid-free situations Figure 2 a as well as in glucose-free situations Figure 2 b. The balance is specially relevant in protein kinetics in preterm infants where amino acids are provided by intravenous solutions [ 66 ]. The autophagic stage is probably deeply affecting the cellular metabolism.
In mammals, autophagy undergoes rhythmic variation in accordance with the feeding cycles. The relationship between autophagy and circadian rhythms has been proposed [ 67 ], but the molecular link between these two phenomena is not yet known.
Cells have to process diverse signals such as temperature, pH, and nutrient concentrations in order to maintain a normal physiology. In vivo, cells are believed to use clock genes to organize and adapt cellular metabolisms and coordinate three-dimensional macromolecular organization their phenotype in a noisy molecular environment molecular signals criss-crossing in and between cells and irrelevant chemical messages.
Exfoliated epithelial cells in anoikis can be seen as a way to obtain chronobiological information dating back to the time of cells leaving the top of the functional units. Signals encoded in the amplitude domain are predominantly based on concentrations of signaling molecules, a parameter difficult to measure on exfoliated cells in anoikis without proper normalization related to the single cell level on highly purified cellular phenotypes.
In addition, some highly labile biochemical modifications like phosphorylation are probably lost during the storage of biological fluids and in the isolation process or can be made irrelevant to the pathophysiology of the mucosa due to the turnover of the signal by the cellular machinery. However, addition of phosphatase inhibitors to cell extracts may preserve period proteins [ 68 ].
Significant improvements in the quality of cellular extracts may be achieved by using extraction buffers suitable to preserve clock gene products. The biological information encoded in the frequency domain of an oscillatory signal can be transmitted as concatenated signals with multiple biologically significant signals to gene behind the regulatory sequence within the promoter.
On transgenic mammals, oscillations can be measured by recording rhythms of light emissions by cells in which the promoter of some clock gene is linked to a luciferase reporter.
On human or nontransgenic mammals, oscillations per se cannot be measured in absence of spectrofluorimetric methods applicable on freshly recovered living cells, but indirect evidence of gene-circuit activation may be recovered. Long-lasting or resilient information may be accessible either through 1 the machinery of transcription at the site of fixation on the DNA of the cells or 2 by the histone code as these epigenetics modifications are believed to be acquired with a stability related to the original tissue [ 69 ] and to the time of day [ 70 ].
The chronobiological information that we can extract from exfoliated epithelial cells depends on the techniques used to isolate cellular material or the manipulation of physiological parameters Figure 1 and on the affinity of interactions of clock molecular components with stable molecules like DNA or the persistence of the physiological effects that they are inducing.
We may speculate that quiescent cells like epithelial gastric cells are retaining fully functional clocks, that is, consistent information with their time at exfoliation and subsequent cell survival out of the organism. The induction of gastric cell exfoliation by nutrient cycle developed in rats [ 5 ] that we have adapted on lactating rat pups [ 43 ] can be used in the future to address questions about the stability of clock information during anoikis.
Exfoliated epithelial cells can be followed by microscopic examination from the initial step of loss of contact at the mouth of the gastric gland to the recovery of cells in the stomach lumen. In addition, the model is clearly relevant to clinical situation in which patients are equipped with nasogastric tubing.
However, there may be tissue-specific differences in the molecular composition of the circadian clock, and clock components that have subtle effects on the central clock function may play a more prominent role in the regulation of peripheral clocks. Yagita et al. The most striking example is the apparent redundancy of clock with its homolog npas2, which are largely equivalent molecules with strict structural differences [ 72 , 73 ].
Exfoliated epithelial cells after loosing contact with extracellular matrix are surviving by activating autophagy. Three main physiological pathways have been described associated to the regulation of autophagy: AKT energy sensing , EGR-R growth factor sensing , and bcl-2 stress-related programmed-cell death. According to Gan et al. Clock components are probably also altered during this process, but there are no data on the relation between autophagy and clock regulation.
By contrast, explants of tissue isolated from transgenic rat for period1 gene is giving some chronobiological information about the chaotic expression of this gene under the drastic external conditions of explantation [ 75 ]. To avoid such chaotic evolution with the loss of chronobiological information, experimenters are using mechanical punches of mucosae which are directly snap frozen in liquid nitrogen. This strategy is a reliable but invasive solution to study clock gene expression in time series.
Otherwise, tissue biopsies can be explanted in culture to derive primary cells or cell lines and record clocks functioning just like with exfoliated cells. However, cell lines have lost contact with body's network, and their clock systems are probably quickly reorganized to tune up with their new in vitro environment [ 76 , 77 ]. In the future, the use of transgenic mice for autophagic gene circuitry will also help to appreciate the exfoliation status and the molecular link between clocks and autophagy [ 78 ].
Exfoliated epithelial cells could be extremely useful to deal with subtle environmental influences during development causing persistent changes in epigenetic regulation. They represent an alternative to fibroblasts which can be easier to collect on adults, and they putatively are giving molecular information from inner tissues difficult to access. The problem in the recovery of exfoliated cells is to relate the cell phenotypes and their physiological status with the intact tissue structure of the donor.
In addition, the degradation of biological information depends on the bioactive compounds present in the biological fluids which can be heavily loaded with enzymes like digestive fluids.
A specific application explored in our laboratory is to develop studies in exfoliation in order to improve nursing care in preterm infants and to prevent the onset of such a syndrome during adult life.
Tracking exfoliated epithelial cells can be used to follow the renewal of the gastric epithelium in order to monitor nutritional or pharmacological practices.
Recently, we have shown that circadian clock genes were disregulated following an episode of perinatal denutrition [ 79 ]. The isolation of exfoliated epithelial cells from pups or infants suffering from perinatal denutrition at the onset of the problem or later in adult life may help to know whether the histone acetyltransferase's activity of CLOCK can be used to explore the stability of epigenetic profile in exfoliated epithelial cells.
However, there is a lack of biomarkers to study exfoliated epithelial cells and the role of clock genes, if any, in autophagy. Among many unsolved questions which can be listed, we can wonder what is the biological information retained, altered, or lost during anoikis?
Future works may focus on the mTOR signaling pathway which has been found downregulated in detached epithelial cells [ 74 ] and, in adipocytes, linked to diurnal gene expression and metabolic regulation [ 80 ]. Recent data on the molecular biology of clock components indicate that central and peripheral clocks differ in their coupling with the different categories of synchronizers as well as in their output on rodent models [ 81 , 82 ] as well as on human data [ 68 ].
A better understanding of exfoliation may be useful not only to translational research but also to tissue reconstruction of mucosa.
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Please enable JavaScript. JavaScript ist in Ihrem Browser deaktiviert. According to their studies serum, saliva and GCF ILA levels are increased in periodontitis patients and correlate with the clinical parameters attachment loss, pocket depth and bleeding on probing.
GAS6 is constitutively expressed in oral epithelial cells and was shown to downregulate epithelial activation at equilibrium state in order to sustain homeostasis This provides a more tolerogenic immunological environment for the oral microbiota GAS6 not only upregulates the expression of adhesion molecules in blood vessels which supports extravasation of immune cells belonging to the innate immune response, it also increases the expression of CCL19 and CCL21 chemokines and thus supports oral DCs to migrate to the lymph nodes.
The authors concluded that GAS6 facilitates migration of inflammatory cells and DCs through the endothelium in both directions, while T-cell stimulation and activation of the mucosa is inhibited. This highly regulated activity of GAS6 supports a rapid but still moderate mucosal immunity to oral pathogens Evidence suggests an increased risk for cancer in chronic infections and inflammation.
Bacterial infections and carcinogenesis seem to be connected Periodontitis, one of the most common chronic human inflammatory diseases, is caused by microorganisms in the oral biofilm that trigger local inflammation.
Periodontitis induces epithelial proliferation and apical migration along the root surface of the tooth and leads to a constant release of inflammatory cytokines, growth factors, prostaglandins, and enzymes, which all of them are closely associated with the development of cancer In previous studies by Tezal et al. High PD-L1 expression has been linked to different types of human malignancies like lung cancer, pancreatic cancer, oral cancer, kidney cancer, breast and gastric cancer , Head and neck cancer belongs to the 10 most frequent cancers worldwide Tumors can only grow if their tissue environment provides them with a milieu that sustains their growth and spread.
Alterations of tissue homeostasis by infection or inflammation can compromise stromal structural integrity and support tumorigenesis Programmed death ligand 1 PD-L1, also called B7-H1 belongs to the B7 family and plays an important role in the regulation of cell-mediated immune response , PD-L1 mediated signals are essential in co-signaling of T cell activation and tolerance PD-L1 signals are also able to downregulate T cell functions and survival , Modification of immune responses in cancer sites is a crucial mechanism that is linked to immune evasion of tumors.
In the tumor microenvironment PD-L1 and programmed death receptor 1 PD-1 may interact and induce tumor-protective mechanisms by activation of multiple specific pathways including ligation of PD-1 by PD-L1 on antigen specific T cells.
Ligation of PD-1 by PD-L1 possibly promotes tolerance and directly protects the tumor from apoptosis by reverse signaling through PD-L1 , , It was demonstrated that P. High levels of PD-L1 were demonstrated in invasive oral squamous carcinoma cells Also, positive PD-L1 expression was detected in tissue samples of oral squamous cell carcinomas ex vivo Membrane proteins of P. Primary human gingival keratinocytes PHGK and oral squamous cell carcinoma SCC cells up-regulated a number of inflammation-related genes upon infection with P.
These data not only suggest that P. In a Chinese population an increased risk for head and neck carcinomas in individuals with oral submucous fibrosis, oral leukoplakia and repetitive dental ulcers was demonstrated suggesting a strong association between these diseases and cancer Also patients with colorectal cancer carry strains of F. The effect of oral pathogens on the development of oral tumors was investigated by Hoppe et al. Stimulation of oral tumor cells with P. Bacteria as well as anti-microbial peptides induced diverse effects on the transcription levels of the oncogenic defensin genes and epidermal growth factor receptor EGFR signaling.
The primary impact of the two oral pathogens were opposite on the proliferation behavior of oral tumor cells. Human defensins differently modify epidermal growth factor receptor signaling, supporting the assumption that these anti-microbial peptides are possible ligands of EGFR.
Interaction of these two molecules may cause the modification of the proliferative behavior of oral tumor cells A newly established model of long term infection by stimulating human immortalized oral epithelial cells HIOECs with P. Persistent infection with P. Furthermore, tumor-related genes including GAS6 and PD-L1 that possibly act as key regulators in transformation from non-cancerous to tumor cells were upregulated as a reaction to long-term exposure of P.
The authors concluded that P. Using a newly-established murine oral tumorigenesis model that is associated with periodontitis, it was reported that chronic bacterial infection supports development of OSCC, inducing enhanced signaling of the IL signal transducer and activator of transcription 3 STAT3 pathway.
The results indicate that periodontal pathogens like P. Furthermore, these pathogens stimulate the proliferation of human OSCC and induce expression of molecular key factors that take part in tumorigenesis, such as STAT3, that becomes activated in response to interferons, EGF, IL-5, IL-6, and cyclin D1, which is required for progression through the G1 phase of the cell cycle and induces cell migration.
These findings represent a function of oral bacteria in the mechanism of chemically induced OSCC tumorigenesis The epithelial—mesenchymal transition EMT is critical in the conversion of normal epithelial cells into carcinoma cells during carcinogenesis.
In a newly established long term infection in vitro model Lee et al. Furthermore, the periodontal pathogens induced augmented activation of Snail and the electrical impedance in comparison with unexposed controls of the cultures was reduced. The capability of the cells to migrate was extended as reaction to bacterial stimulation, demonstrated by the number of migrating cells and scratch-wound closure rates.
In conclusion, persistent stimulation of primary rat oral keratinocyte cultures to periodontal pathogens elicited EMT-like properties, which indicates that this process may promote loss of epithelial integrity The composition of the gingival epithelial barrier is quite complex since its structure composes of a huge number of different molecules.
Keratins are the major component of the keratinizing stratified epithelial cytoskeleton. Depending on localization and function different epithelia express a distinct cytokeratin pattern. In order to sustain their function, stratified epithelia, including the oral mucosa, have to sustain tight cell-cell adhesion in the viable cells that involves intercellular tight and adherens junctions which connect to the actin cytoskeleton.
Oral tissue immune response is able to recognize microbial infection and colonization and is able to manage it. The epithelial cells express a number of pattern recognition receptors, including TLRs, NOD1, NOD2 and PARs and are able to assemble different kinds of inflammasomes and express a variety of pro-inflammatory cytokines and chemokines.
Resident oral bacteria permanently influence epithelial host cells. Depending on their composition biofilms differentially modify cellular immune responses of the epithelium. Major periodontal pathogens like P. The balanced immune-inflammatory state of the host with its biofilm in health may be disturbed by distinct species, such as P.
Chronic infections and persistent inflammation are associated with an increased risk of cancer. Persisting bacterial agents may induce up-regulation of immune-inhibitory receptors which in turn facilitate the ability of cancer cells to evade from anti-tumor immune responses of the host. Furthermore, long term infection possibly supports carcinogenesis by regulating gene expressions of the infected epithelial cells in a way that leads to development into a phenotype indicating cellular transformation from normal to cancerous.
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Provost E, Rimm DL. Understanding how the small intestine functions requires looking at the structure of the mucosa in more detail. The mucosa of small intestinal mucosa is arranged into two fundamental structures: Villi are projections into the lumen covered predominantly with mature, absorptive enterocytes, along with occasional mucus-secreting goblet cells. These cells live only for a few days, die and are shed into the lumen to become part of the ingesta to be digested and absorbed.
That's right, we're all really cannibals. Crypts of Lieberkuhn are moat-like invaginations of the epithelium around the villi, and are lined largely with younger epithelial cells which are involved primarily in secretion. Importantly, toward the base of the crypts are stem cells , which continually divide and provide the source of all the epithelial cells in the crypts and on the villi.
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