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PubMed2004

[Relationship between epithelial-immunologic cells transdifferentiation and pseudoepitheliomatous granuloma lesion].

OBJECTIVE: Inappropriate treatment at early stage of wound could result in the formation of pseudoepitheliomatous granuloma (PEG). The correlation of abnormal transdifferentiation of epithelial cells to immunologic cells and the occurrence of PEG lesion was investigated. METHODS: Morphological change of epithelial tissue was observed with histopathology in 11 specimens of PEG lesions and 6 specimens of normal skins from PEG edge (PEG-N) from 11 patients with damaged skin. The expression characteristics and distribution of pan-cytokeratin (CKp), IV type collagen, laminin (LM), epithelial cadherin (E-Cad), beta-catenin (beta-Cat), focal adhesion kinase (FAK), stem cell factor (SCF) and its receptor-c-Kit, proliferating cell nuclear antigen(PCNA), and cluster of differentiation-14 (CD14), CD68 and mast cell tryptase (MCT) in PEG were detected with the immunohistochemical and the indirect immunofluorescent double-staining. RESULTS: In comparison with PEG-N, epithelial tissue take on squamous metaplasia, and stroma was infiltrated with intensive microvessels and inflammatory cells in the PEG lesion. Poor epithelial basal layer constitution, basal polarization, and migration of basal cells to stroma could be observed. In the ultrastructure, the loose intercellular junction of basal cells and the increased nucleus/cytoplasm ratio and intercellular space could be observed, neonatal monocytoid cells and macrophages and mast cells as a exuviate-like manner brooded from cytoplasm of original epithelial cells and basement membrane. protein expression of CKp and E-Cad by basal cells was significantly decreased, and the IV type collagen and LM protein could not be found in basement membrane of identical locus. By contrast, the immunoreactivity of beta-Cat and FAK was apparently increased. In addition, CD14(+) monocytes, CD68(+) macrophages, MCT(+) mast cells and CD68(+)/MCT(+) cells with various size, and these cells of stronger immuno-staining of SCF, c-Kit and PCNA antigen could be found in epithelial tissue and stroma. CONCLUSION: Epithelial cells in PEG related to wound are characteristized by transdifferentiation of epithelial cells to immunologic cells, wich may be associated with local infectious and inflammatory reaction, ultimately resulting in enhancement the ratio of beta-Cat/E-Cad signal and activation SCF-c-Kit signal pathway. The phenomena of transdifferentiation epithelial cells in the PEG lesion will help to recognize of the neoplatic immune and trauma repair mechanism.

Adolescent↗
PubMed1995

[Studies on the cell models of differentiation reversal phenotypes of human rhabdomyosarcoma].

We have observed the features of malignant phenotypes in human rhabdomyosarcoma RD cells. These cells exhibited high growth rate, aberrant relation between cell proliferation and myogenic terminal differentiation, blockage of myofibrillogenesis, inhibition of gap junctional intercellular communication (GJIC) and inhibition of transcriptional expression of gap junction gene, connexin 43 (Cx43). By utilization of single cell subclone separation and cDNA cell transfection techniques, we obtained several RD subclones, among them 3 were representative of differences in phenotypes and were selected for further study. They were single-cell subclone RDL6, RDL3, and a Cx43 transfectant clone of RDL6, the RDL6/C-4. Through determination of cell growth doubling time, co-stain of 3H-TdR autoradiography with myosin heavy chain (MHC) immunofluorescence, immunofluorescent cytochemical examination and slot-blot analysis, it was demonstrated that significant differences existed between each of the 3 subclones. They were differnet in cell growth rate, cell proliferation and terminal differentiation coupling relation, progress of myogenesis, functional expression of Cx43 gene, and expression of proto-oncogenes, c-myc, Ha-ras and c-met products, therefore they could be used as cell models in the study of reverse transformation of rhabdomyosarcomas. The reversal differentiation markers, their examination approaches and practical value were discussed.

Cell Transformation, Neoplastic↗
PubMed1991

Alterations in intercellular communication during the stage of promotion.

The promotion stage is a crucial step in the process of carcinogenesis. During this stage, the initiated cell population is clonally expanded to morphologically discriminable forms. Exogenous or endogenous agents that influence this clonal expansion have tumor-promoting activity. Inhibition of gap junctional intercellular communication is one of a number of cellular changes seen in cells after exposure to promoting agents. GJIC can be inhibited through either modification of intracellular control mechanism or through transcriptional or translational down-expression of the gap junction protein. Through either mechanism, the net effect is a decrease in GJIC by tumor promoters. This decrease in GJIC, while occurring in normal cells and preneoplastic cells alike, appears to be more efficacious in the preneoplastic cells, and appears to prevent GJIC between the preneoplastic cells and the normal surrounding hepatocytes. This isolation of the preneoplastic cells by hepatic tumor promoters from the normal surrounding hepatocytes may separate the preneoplastic cells from growth regulatory control of the normal liver, thus allowing the preneoplastic cells to clonally expand by cell proliferation. Whether the disruption of GJIC and down-regulation of gap junction protein expression seen in hepatic foci by exposure to tumor promoters are causes or effects of the resulting cell proliferation remains to be determined. Certainly, the modification of GJIC and the expression of the gap junction protein by tumor promoters are important cellular changes that produce a phenotypically altered population of hepatocytes.

Animals↗
PubMed2002

Intercellular communication, homeostasis, and toxicology.

The article highlighted in this issue is "Inhibition of Gap Junctional Intercellular Communication by Perfluorinated Compounds in Rat Liver and Dolphin Kidney Epithelial Cell Lines in Vitro and Sprague-Dawley Rats in Vivo" by W. Hu, P. D. Jones, B. L. Upham, J. E. Trosko, C. Lau, and J. P. Giesy (pp. 429-436).

Animals↗
PubMed1979

Occluding-like junctions at mesaxons of central myelin in Anolis carolinensis are not 'tight'. A freeze-fracture-protein tracer analysis.

The junctional complexes of the myelin sheath of central nervous system axons in the American chameleon, Anolis carolinensis, exhibit an intramembrane ridge and groove construction in freeze-fracture replicas that has usually been interpreted in other organisms as evidence for an occluding or tight intercellular junction. Close examination of PF fracture face ridges, however, shows them to be made up of discontinuous rows of particles of variable length separated by frequent gaps of non-uniform width. Introduction of horseradish peroxidase into the intercellular milieu of the lizard central nervous system is followed by appearance of this protein in interlamellar spaces of the myelin sheath and in the intercellular spaces containing focal membrane fusions that correspond precisely in position and center-to-center spacing to the ridges and grooves in platinum replicas of the same tissue. Since the junctional ridges on PF fracture faces in these mesaxonal junctional complexes are conspicuously discontinuous and since the areas within the myelin sheath where these junctional complexes are located inner and outer mesaxons) are readily permeated by exogenous protein tracer, it is concluded that the junctional complexes of central myelin mesaxons, heretofore incorrectly interpreted as functionally tight, are actually very leaky and probably contribute only to the structural stability of the myelin sheath architecture.

Animals↗
PubMed1981

Induction of cell--cell channel formation by mRNA.

Intercellular junctional communication is very common in normal organized tissue. It provides a pathway for transmission of electrical signals, especially in heart muscle, and may be important in differentiation and growth control. The hydrophilic channels which enable cell--cell communication have been well characterized by biophysical methods, and there is now good evidence that they are contained in the nexus (gap junctions). Little, however, is known about the molecular mechanism of biosynthesis of junctional channels. Knowledge in this area has been obtained almost exclusively from experiments with reaggregated cells, a system complicated by the fact that de novo synthesis of channel proteins is obscured by reassembly of pre-existing subunits or utilization of precirsors. To avoid these problems, we have now isolated mRNA from cells that are in the process of making new intercellular nexus with high efficiency, incorporated it via liposomes into communication-defective cells and have shown that the recipient cells established junctional communication.

Animals↗
PubMed2000

Effect of tumor-conditioned medium on intercellular communication and proliferation of Balb/c 3T3 cells.

The possible role of tumor cell-derived factors in the regulation of gap junctional intercellular communication and proliferation of fibroblasts was studied in a model system of Balb/c 3T3 cells growing in tumor conditioned medium by Lucifer Yellow CH dye-transfer and BrdU incorporation assays. Six to 24 h incubation of Balb/c 3T3 cells in a medium conditioned by WiDr adenocarcinoma cells enhanced the gap junctional communication between the cells by 25-40% as revealed by intercellular transfer of a fluorescent dye Lucifer Yellow CH. Simultaneously the cell proliferation rates were examined and found to be reduced by 23% at 24 h treatment. Since adenocarcinoma cells are known to secrete different growth factor-like polypeptides into their conditioned medium, we suppose that tumors that produce these molecules might alter their host environment through the enhancement of cell-cell communication thereby facilitating the exchange of modulatory factors.

3T3 Cells↗
PubMed2000

Differential effect of subcellular localization of communication impairing gap junction protein connexin43 on tumor cell growth in vivo.

There is a large body of evidence suggesting the connexin gap junction proteins appear to act as tumor suppressors, and their tumor inhibitory effect is usually attributed to their main function of cell coupling through gap junctions. However, some cancer cells (e.g. the rat bladder carcinoma BC31 cell line) are cell-cell communication proficient. Using specific site-directed mutagenesis in the third membrane-spanning (3M) domain of connexin43 (Cx43), we abolished the intrinsic gap junction intercellular communication (GJIC) in BC31 cells either by closing the gap junctional channels or by disruption of the transport of connexin complexes to the lateral membrane. Clones of BC31 cells transfected with a dominant negative Cx43 mutant giving rise to gap junctional channels, permeable only for a small tracer (neurobiotin), displayed accelerated growth rate in vivo, showing the critical role of selective gap junctional permeability in the regulation of cell growth in vivo. The use of other dominant-negative mutants of Cx43 also suggested that the effect of impaired communication on the tumorigenicity of cancer cells depends on the subcellular location of connexin. Inhibition of intrinsic GJIC in BC31 cells by sequestering of Cx protein inside the cytoplasm, due to expression of dominant-negative transport-deficient Cx43 mutants, did not significantly enhance the growth of transfectants in nude mice, but occasionally slightly retarded it. In contrast, augmentation of GJIC in BC31 cells by forced expression of wild-type Cx43, or a communication-silent mutant, fully suppressed tumorigenicity of these cells. Overall, these results show that cell coupling is a strong, but not the sole, mechanism by which Cx suppresses growth of tumorigenic cells in vivo; a GJIC-independent activity of Cx proteins should be considered as another strong tumor-suppressive factor.

Animals↗
PubMed2006

VCAM-1 inhibits TGFbeta stimulated epithelial-mesenchymal transformation by modulating Rho activity and stabilizing intercellular adhesion in epicardial mesothelial cells.

Regulation of epithelial-mesenchymal transformation (EMT) is of central importance both in normal development and in disease. During heart development, cells of the superficial epicardial mesothelium undergo EMT to give rise to precursor cells of the coronary vasculature and cardiac fibroblasts. Here we report that the alpha(4)beta(1) integrin ligand, VCAM-1, inhibits EMT of chick epicardial mesothelial cells stimulated by TGFbeta isoforms. We further investigated the molecular basis of this inhibition using cultured chick embryonic and rat adult epicardial mesothelial cells. We observed that VCAM-1 increased cortical actin filaments at intercellular junctions and reduced stress fibers across epicardial cells. VCAM-1 inhibited stress fiber formation by TGFbeta1, TGFbeta2, TGFbeta3 and lysophosphatidic acid and altered Rho activity stimulated by TGFbeta3. This was accompanied by an increase in tyrosine phosphorylation of p190RhoGAP. All three TGFbeta isoforms weakened intercellular adhesion, reduced membrane localization of beta-catenin and E-cadherin and stimulated epicardial EMT in chick hearts. Each of these effects was restricted by simultaneous VCAM-1 treatment. Our data support the hypothesis that VCAM-1 can alter epicardial EMT at two key points: it limits Rho-dependent events such as stress fiber formation and it maintains the association of beta-catenin and E-cadherin with the adherens junction.

Actin Cytoskeleton↗
PubMed1994

Cell culture assays for chemicals with tumor-promoting or tumor-inhibiting activity based on the modulation of intercellular communication.

The ability of chemicals with tumor-promoting or tumor-inhibiting activity to modulate gap junctional intercellular communication is reviewed. The two most extensively used types of assays for screening tests are (1) metabolic cooperation assays involving exchange between cells of precursors of nucleic acid synthesis and (2) dye-transfer assays that measure exchange of fluorescent dye from loaded cells to adjacent cells. About 300 substances of different biological activities have been studied using various assays. For tumor promoters/epigenetic carcinogens, metabolic cooperation assays have a sensitivity of 62% and dye-transfer assays 60%. Thirty percent of DNA-reactive carcinogens also possess the ability to uncouple cells. The complete estimation of the predictive power of these assays could not be made because the majority of the substances studied for intercellular communication effects in vitro have not yet been studied for promoting activity in vivo. Both metabolic cooperation assays and dye transfer assays respond well to the following classes of substances: phorbol esters, organochlorine pesticides, polybrominated biphenyls, promoters for urinary bladder, some biological toxins, peroxisome proliferators, and some complex mixtures. Results of in vitro assays for such tumor promoters/nongenotoxic carcinogens, such as some bile acids, some peroxides, alkanes, some hormones, mineral dusts, ascorbic acid, okadaic acid, and benz(e)pyrene, do not correlate with the data of in vivo two-stage or complete carcinogenesis. Enhancement of intercellular communication was found for 18 chemicals. Among these, cAMP, retinoids, and carotenoids have demonstrated inhibition of carcinogenesis. We examine a number of factors that are important for routine screening, including the requirement for biotransformation for some agents to exert effects on gap junctions. We also discuss the mechanisms of tumor promoter and tumor inhibitor effects on gap junctional permeability, including influences of protein kinase activation, changes in proton and Ca2+ intracellular concentrations, and effects of oxy radical production.

Animals↗
PubMed2004

Functional characterization of Cx43 based gap junctions during spermatogenesis.

In the testis, spermatogenesis is a highly regulated process that includes germ cell multiplication and differentiation supported by Sertoli cells. Gap junction intercellular communication (GJIC), that is known to play an important role in the control of cell proliferation and differentiation, allows communication between adjacent cells. Gap junctions are present within the seminiferous epithelium but the precise nature of coupled cells is not yet identified. By applying a dye-transfer assay to testis, we demonstrated that coupling was basally located in the tubular compartment between adjacent Sertoli cells, between Sertoli cells and spermatogonia and early and late spermatocytes, but not between Sertoli cells and spermatids. Furthermore, no dye transfer occurred from germ cells to Sertoli cells. Specificity of the gap junction coupling was verified with known gap junction inhibitors such as oleamide, heptanol, and glycyrrhetinic acid. We developed a sophisticated assay that allows correlating the in vivo dye transfer with cell morphological identification and Cx43 expression. This approach demonstrated the Cx43 participation in the coupling. Interestingly Cx43 expression and dye-coupling varied with the stages of spermatogenesis. Our results suggest that Cx43 based gap junctions form a transversal and longitudinal intercellular communication network within seminiferous tubules, and that specific communication territories are formed within the seminiferous tubules to ensure the synchronization of germ cell proliferation and differentiation.

Animals↗
PubMed2000

Enhancing paracellular permeability by modulating epithelial tight junctions.

The intestinal epithelium is a major barrier to the absorption of hydrophilic drugs. The presence of intercellular junctional complexes, particularly the tight junctions (zona occludens), renders the epithelium impervious to hydrophilic drugs, which cannot diffuse across the cells through the lipid bilayer of the cell membranes. There have been significant advances in understanding the structure and cellular regulation of tight junctions over the past decade. This article reviews current knowledge regarding the physiological regulation of tight junctions and paracellular permeability, and recent progress towards the rational design of agents that can effectively and safely increase paracellular permeability via modulation of tight junctions.

Journal Article↗
PubMed1998

In vitro and in vivo effects of retrovirus-mediated transfer of the connexin 43 gene in malignant gliomas: consequences for HSVtk/GCV anticancer gene therapy.

In tumors, gap junctional intercellular communication (GJIC) is usually down-regulated and the expression of connexins, membrane proteins constituting gap junction channels, is often low or altered. GJIC, allowing the intercellular diffusion of ganciclovir (GCV) triphosphate, is also one mediator of the 'bystander effect', the phenomenon by which herpes simplex virus thymidine kinase (HSVtk)-transduced, neoplastic cells kill surrounding HSVtk-negative cells when treated with GCV. We set up experiments to evaluate the effects of retrovirus-mediated in vivo gene transfer of connexin 43 in malignancies with low GJIC capacity. We found that U-87 human glioblastoma cells transfected in vitro by the human Cx43 cDNA grow significantly more slowly than control U-87 cells and lose their tumorigenicity when injected subcutaneously in nude mice. When the Cx43 gene was transduced in vitro in U-87 cells by a retroviral producer cell line (N3.2.ii, titer 1.5 x 10(6) c.f.u./ml) in vivo results were similar. However, only when U-87 cells were co-injected with N3.2.ii cells in nude mice in a 1:5 ratio, a 50% reduction in tumor size was obtained during the first 3 weeks. Moreover the coinjection of U-87 cells with N3.2.ii and SBA cells (a retroviral producer cell line expressing the HSVtk gene), was not able to potentiate the effects of GCV administration, suggesting that Cx43 gene transfer requires more efficient vectors to increase the bystander effect in vivo.

Animals↗
PubMed1999

Stress fiber networks in sinus endothelial cells in the rat spleen.

The wall of the splenic sinus is well known to be a critical site in the control of the blood-cell passage through the splenic cord. However, there is little information on what mechanism controls the blood-cell passage between the sinus endothelial cells adhered with intercellular junctions. Stress fibers of sinus endothelial cells in the rat spleen were examined by transmission electron microscopy and immunofluorescence microscopy. After extraction with saponin, the stress fibers were found to be conspicuously electron-dense in the basal portion of the cells and demonstrated two characteristic types and the mixed type of these. One type of the stress fibers was corrugated and formed thick, electron-dense bundles, and the other type had straight bundles with electron-dense areas at intervals. Statistically, the lengths of two types of stress fibers are significantly different. Although most of the stress fibers were segmented by the ring fibers, some of them ran successively beyond the attachment site of the ring fibers and thus stretched longitudinally and tangentially in the basal part of the cell to form a widespread network. The peripheries of the networks were attached to the basal plasma membrane at the ring fibers and the lateral membranes at the focal adhesions and the cell-cell adherens junction, respectively. Phosphotyrosine is localized in the basal part and at the intercellular adhesion site of the endothelial cells. Two types of stress fibers were organized in the sinus endothelial cells, and they form a widespread network. The possibility might be considered that stress fibers play important roles in the signal transduction and the regulation of cellular attachment and detachment.

Animals↗
PubMed1992

Clostridium difficile toxin B disrupts the barrier function of T84 monolayers.

The contribution of toxin B to Clostridium difficile-associated infection is undefined. Toxin B induces dramatic phenotypic alterations (cytotoxic effects) in cultured mesenchymal and nonintestinal epithelial cells, yet its effects on intestinal epithelial cells are not clearly understood. The alterations induced by toxin B in nonintestinal cells appear to be secondary to toxin-induced redistribution of filamentous actin. It has not been determined whether toxin B exerts similar effects on cultured intestinal epithelial cells or whether such phenotypic alterations are of any physiological consequence. To address these questions, we examined the effect of C. difficile toxin B on the phenotype and barrier function of T84 cell monolayers. Our studies show that the cytotoxic effects of toxin B, i.e., cell rounding, do extend to cultured intestinal epithelial cells (T84). In addition, toxin B dramatically reduces the barrier function of T84 monolayers grown on collagen-coated filters. Toxin B-induced redistribution of filamentous actin appears to be responsible for the alterations in both intestinal epithelial cell phenotype and barrier function. Specifically, filamentous actin comprising the perijunctional actomyosin ring, known to be important in regulating tight junction permeability, is condensed into discrete plaques. Flux studies confirm that the permeability defect is at the level of the tight junction. We conclude that toxin-induced changes in actin distribution perturb intercellular junctional contacts and thereby ablate epithelial barrier function. There was no evidence of cell death as determined by lactate dehydrogenase release assays.

Actins↗
PubMed2004

aPKC acts upstream of PAR-1b in both the establishment and maintenance of mammalian epithelial polarity.

BACKGROUND: aPKC and PAR-1 are required for cell polarity in various contexts. In mammalian epithelial cells, aPKC localizes at tight junctions (TJs) and plays an indispensable role in the development of asymmetric intercellular junctions essential for the establishment and maintenance of apicobasal polarity. On the other hand, one of the mammalian PAR-1 kinases, PAR-1b/EMK1/MARK2, localizes to the lateral membrane in a complimentary manner with aPKC, but little is known about its role in apicobasal polarity of epithelial cells as well as its functional relationship with aPKC. RESULTS: We demonstrate that PAR-1b is essential for the asymmetric development of membrane domains of polarized MDCK cells. Nonetheless, it is not required for the junctional localization of aPKC nor the formation of TJs, suggesting that PAR-1b works downstream of aPKC during epithelial cell polarization. On the other hand, aPKC phosphorylates threonine 595 of PAR-1b and enhances its binding with 14-3-3/PAR-5. In polarized MDCK cells, T595 phosphorylation and 14-3-3 binding are observed only in the soluble form of PAR-1b, and okadaic acid treatment induces T595-dependent dissociation of PAR-1b from the lateral membrane. Furthermore, T595A mutation induces not only PAR-1b leakage into the apical membrane, but also abnormal development of membrane domains. These results suggest that in polarized epithelial cells, aPKC phosphorylates PAR-1b at TJs, and in cooperation with 14-3-3, promotes the dissociation of PAR-1b from the lateral membrane to regulate PAR-1b activity for the membrane domain development. CONCLUSIONS: These results suggest that mammalian aPKC functions upstream of PAR-1b in both the establishment and maintenance of epithelial cell polarity.

Animals↗
PubMed2001

Members of the Jagged/Notch gene families are expressed in injured arteries and regulate cell phenotype via alterations in cell matrix and cell-cell interaction.

The Jagged/Notch signaling pathways control cell fate determination and differentiation, and their dysfunction is associated with human pathologies involving cardiovascular abnormalities. To determine the presence of these genes during vascular response to injury, we analyzed expression of Jagged1, Jagged2, and Notch1 through 4 after balloon catheter denudation of the rat carotid artery. Although low levels of Jagged1, Jagged2, and constitutive expression of Notch1 were seen in uninjured endothelium, expression of all was significantly increased in injured vascular cells. High Jagged1 expression was restricted to the regenerating endothelial wound edge, whereas Notch transcripts were abundant in endothelial and smooth muscle cells. To understand the basis for Jagged/Notch control of cellular phenotype, we studied an in vitro model of NIH3T3 cells transfected with a secreted form of the extracellular domain of Jagged1. We report that the soluble Jagged1 protein caused decreased cell-matrix adhesion and cell migration defects. Cadherin-mediated intercellular junctions as well as focal adhesions were modified in soluble Jagged1 transfectants, demonstrating that cell-cell contacts and adhesion plaques may be targets of Jagged/Notch activity. We suggest that Jagged regulation of cell-cell and cell-matrix interactions may contribute to the control of cell migration in situations of tissue remodeling in vivo.

3T3 Cells↗
PubMed2006

Listeria monocytogenes invades the epithelial junctions at sites of cell extrusion.

Listeria monocytogenes causes invasive disease by crossing the intestinal epithelial barrier. This process depends on the interaction between the bacterial surface protein Internalin A and the host protein E-cadherin, located below the epithelial tight junctions at the lateral cell-to-cell contacts. We used polarized MDCK cells as a model epithelium to determine how L. monocytogenes breaches the tight junctions to gain access to this basolateral receptor protein. We determined that L. monocytogenes does not actively disrupt the tight junctions, but finds E-cadherin at a morphologically distinct subset of intercellular junctions. We identified these sites as naturally occurring regions where single senescent cells are expelled and detached from the epithelium by extrusion. The surrounding cells reorganize to form a multicellular junction that maintains epithelial continuity. We found that E-cadherin is transiently exposed to the lumenal surface at multicellular junctions during and after cell extrusion, and that L. monocytogenes takes advantage of junctional remodeling to adhere to and subsequently invade the epithelium. In intact epithelial monolayers, an anti-E-cadherin antibody specifically decorates multicellular junctions and blocks L. monocytogenes adhesion. Furthermore, an L. monocytogenes mutant in the Internalin A gene is completely deficient in attachment to the epithelial apical surface and is unable to invade. We hypothesized that L. monocytogenes utilizes analogous extrusion sites for epithelial invasion in vivo. By infecting rabbit ileal loops, we found that the junctions at the cell extrusion zone of villus tips are the specific target for L. monocytogenes adhesion and invasion. Thus, L. monocytogenes exploits the dynamic nature of epithelial renewal and junctional remodeling to breach the intestinal barrier.

Journal Article↗