Porcine Intestinal Epithelial Cell Line Research Articles

Porcine epidemic diarrhea virus N protein prolongs S-phase cell cycle, induces endoplasmic reticulum stress, and up-regulates interleukin-8 expression

Porcine epidemic diarrhea (PED) is an acute and highly contagious enteric disease of swine caused by porcine epidemic diarrhea virus (PEDV). The porcine intestinal epithelial cell is the PEDV target cell. In this study, we established a porcine intestinal epithelial cell (IEC) line which can stably express PEDV N protein. We also investigate the subcellular localization and function of PEDV N protein by examining its effects on cell growth, cycle progression, interleukin-8 (IL-8) expression, and survival. The results show that the PEDV N protein localizes in the endoplasmic reticulum (ER), inhibits the IEC growth and prolongs S-phase cell cycle. The S-phase is prolonged which is associated with a decrease of cyclin A transcription level and an increase of cyclin A degradation. The IEC expressing PEDV N protein can express higher levels of IL-8 than control cells. Further studies show that PEDV N protein induces ER stress and activates NF-κB, which is responsible for the up-regulation of IL-8 and Bcl-2 expression. This is the first report to demonstrate that PEDV N protein can induce cell cycle prolongation at the S-phase, ER stress and up-regulation interleukin-8 expression. These findings provide novel information on the function of the PEDV N protein and are likely to be very useful in understanding the molecular mechanisms responsible for PEDV pathogenesis.

Analyses of intestinal commensal Escherichia coli strains from wild boars suggest adaptation to conventional pig production conditions

To test the hypothesis that Escherichia coli populations have adapted to conventional pig production practices, we comparatively tested intestinal commensal E. coli from wild boars versus isolates from domestic pigs by analyzing virulence-associated factors, adhesion, and metabolic activities.Virulence-associated genes typical for intestinal pathogenic E. coli (inVAGs) were sporadically detected among E. coli from wild boars except the adhesion-related gene paa and the enterotoxin-encoding gene astA. In contrast, several VAGs typical for extraintestinal pathogenic E. coli (exVAGs) were common in E. coli from wild boars. The exVAG chuA occurred more often in E. coli from wild boars compared to E. coli from domestic pigs. 23.5% of E. coli from wild boars belonged to EcoR group B2 which is higher than observed for E. coli from clinically healthy domestic pigs. Furthermore, E. coli from wild boars were more efficient in fermentation of carbohydrate sources (dulcitol, inositol, d-sucrose, d-tagatose), and adhered better to the intestinal porcine epithelial cell line IPEC-J2.In conclusion, our findings point towards an adaptation of porcine intestinal E. coli to a specific intestinal milieu caused by different animal living conditions.

Characterization of a porcine intestinal epithelial cell line for influenza virus production

We have developed a porcine intestine epithelial cell line, designated SD-PJEC for the propagation of influenza viruses. The SD-PJEC cell line is a subclone of the IPEC-J2 cell line, which was originally derived from newborn piglet jejunum. Our results demonstrate that SD-PJEC is a cell line of epithelial origin that preferentially expresses receptors of oligosaccharides with Sia2-6Gal modification. This cell line is permissive to infection with human and swine influenza A viruses and some avian influenza viruses, but poorly support the growth of human-origin influenza B viruses. Propagation of swine-origin influenza viruses in these cells results in a rapid growth rate within the first 24 h post-infection and the titres ranged from 4 to 8 log(10) TCID(50) ml(-1). The SD-PJEC cell line was further tested as a potential alternative cell line to Madin-Darby canine kidney (MDCK) cells in conjunction with 293T cells for rescue of swine-origin influenza viruses using the reverse genetics system. The recombinant viruses A/swine/North Carolina/18161/02 (H1N1) and A/swine/Texas/4199-2/98 (H3N2) were rescued with virus titres of 7 and 8.25 log(10) TCID(50) ml(-1), respectively. The availability of this swine-specific cell line represents a more relevant substrate for studies and growth of swine-origin influenza viruses.

Gene Regulation of Intestinal Porcine Epithelial Cells IPEC-J2 Is Dependent on the Site of Deoxynivalenol Toxicological Action

The intestinal epithelial cell layer represents the border between the luminal and systemic side of the gut. The decision between absorption and exclusion of substances is the quintessential function of the gut and varies along the gut axis. Consequently, potentially toxic substances may reach the basolateral domain of the epithelial cell layer via blood stream. The mycotoxin deoxynivalenol (DON) is a Fusarium derived secondary metabolite known to enter the blood stream and displaying a striking toxicity on the basolateral side of polarised epithelial cell layers in vitro. Here we analysed potential mechanisms of apical and basolateral DON toxicity reflected in the gene expression. We used the jejunum-derived, polarised intestinal porcine epithelial cell line IPEC-J2 as an in vitro cell culture model. Luminal and systemic DON challenge of the epithelial cell layer was mimicked by a DON application from the apical or basolateral compartment of membrane inserts for 72 h. We compared the genome-wide gene expression of untreated and DON-treated IPEC-J2 cells with the GeneChip® Porcine Genome Array of Affymetrix. Low basolateral DON (200 ng/mL) application triggered 10 times more gene transcripts in comparison to the corresponding apical application (2539 versus 267) despite the intactness of the challenged cell layer as measured by transepithelial electrical resistance. Analysis of the regulated genes by bioinformatic resource DAVID identified several groups of biochemical pathways modulated by concentration and orientation of DON application. Selected genes representing pathways of the cellular metabolism, information processing and structural design were analysed in detail by quantitative PCR. Our findings clearly show that apical and basolateral challenge of epithelial cell layers trigger different gene response profiles paralleled with a higher susceptibility towards basolateral challenge. The evaluation of toxicological potentials of mycotoxins should take this difference in gene regulation dependent on route of application into account.

Toll-like receptor-2-activating bifidobacteria strains differentially regulate inflammatory cytokines in the porcine intestinal epithelial cell culture system: finding new anti-inflammatory immunobiotics

A total of 23 strains of bifidobacteria taxonomically belonging to five species were tested for their potent immunomodulatory effect using a combination of two methods: the NF-κB-reporter assay using a toll-like receptor 2-expressing transfectant (HEK(pTLR2) system) and the mitogenic assay using porcine Peyer's patches immunocompetent cells. Among the four preselected strains from different immunomodulatory groups, Bifidobacterium breve MCC-117 was able to efficiently modulate the inflammatory response triggered by enterotoxigenic Escherichia coli (ETEC) in a porcine intestinal epithelial (PIE) cell line. Moreover, using PIE cells and swine Peyer's patches immunocompetent cell co-culture system, we demonstrated that the immunoregulatory effect of B. breve MCC-117 was related to the capacity of the strain to influence PIE and immune cell interactions, leading to the stimulation of regulatory T cells. The results suggested that bifidobacteria that express high activity in both the HEK(pTLR2) and the mitogenic assays may behave like potential anti-inflammatory strains. The combination of the HEK(pTLR2) system, the evaluation of mitogenic activity and PIE cells will be of value for the development of new immunologically functional foods and feeds that could prevent inflammatory intestinal disorders. Although our findings should be proven in appropriate experiments in vivo, the results of the present work provide a scientific rationale for the use of B. breve MCC-117 to prevent ETEC-induced intestinal inflammation.

Influence of dietary ingredients on in vitro inflammatory response of intestinal porcine epithelial cells challenged by an enterotoxigenic Escherichia coli (K88)

Enterotoxigenic Escherichia coli (ETEC) K88 is the main bacterial cause of diarrhea in piglets around weaning and the adhesion of ETEC to the intestinal mucosa is a prerequisite step for its colonization. In this study, the adhesion of a fimbriated ETEC and a non-fimbriated E. coli (NFEC) to the intestinal cells and the activation of the innate immune system were evaluated using a porcine intestinal epithelial cell line (IPEC-J2). The impact of several feedstuffs (wheat bran (WB); casein glycomacropeptide (CGMP); mannan-oligosaccharides (MOS); locust bean extract (LB) and Aspergillus oryzae fermentation extract (AO)) on ETEC attachment and the inflammatory response were also studied. The gene expression of TLR-4; TLR-5; IL-1β; IL-8; IL-10 and TNF-α were quantified using Cyclophilin-A, as a reference gene, and related to a non-challenged treatment. The fimbriated strain was markedly better than the non-fimbriated strain at adherence to intestinal cells and inducing an inflammatory response. All the feedstuffs studied were able to reduce the adhesion of ETEC, with the greatest decrease with CGMP or MOS at highest concentration. Regarding the inflammatory response, the highest dose of WB promoted the lowest relative expression of cytokines and chemokines. All tested feedstuffs were able to reduce the adhesion of ETEC to IPEC-J2 and interfere on the innate inflammatory response; however WB should be further studied according to the beneficial results on the intestinal inflammatory process evidenced in this study.

Vulnerability of Polarised Intestinal Porcine Epithelial Cells to Mycotoxin Deoxynivalenol Depends on the Route of Application

Background and AimsDeoxynivalenol (DON) is a Fusarium derived mycotoxin, often occurring on cereals used for human and animal nutrition. The intestine, as prominent barrier for nutritional toxins, has to handle the mycotoxin from the mucosa protected luminal side (apical exposure), as well as already absorbed toxin, reaching the cells from basolateral side via the blood stream. In the present study, the impact of the direction of DON exposure on epithelial cell behaviour and intestinal barrier integrity was elucidated.MethodsA non-transformed intestinal porcine epithelial cell line (IPEC-J2), cultured in membrane inserts, serving as a polarised in vitro model to determine the effects of deoxynivalenol (DON) on cellular viability and tight junction integrity.ResultsApplication of DON in concentrations up to 4000 ng/mL for 24, 48 and 72 hours on the basolateral side of membrane cultured polarised IPEC-J2 cells resulted in a breakdown of the integrity of cell connections measured by transepithelial electrical resistance (TEER), as well as a reduced expression of the tight junction proteins ZO-1 and claudin 3. Epithelial cell number decreased and nuclei size was enlarged after 72 h incubation of 4000 ng/mL DON from basolateral. Although necrosis or caspase 3 mediated apoptosis was not detectable after basolateral DON application, cell cycle analysis revealed a significant increase in DNA fragmentation, decrease in G0/G1 phase and slight increase in G2/M phase after 72 hours incubation with DON 2000 ng/mL.ConclusionsSeverity of impact of the mycotoxin deoxynivalenol on the intestinal epithelial barrier is dependent on route of application. The epithelium appears to be rather resistant towards apical (luminal) DON application whereas the same toxin dose from basolateral severely undermines barrier integrity.

Deoxynivalenol Impairs Porcine Intestinal Barrier Function and Decreases the Protein Expression of Claudin-4 through a Mitogen-Activated Protein Kinase-Dependent Mechanism ,

Deoxynivalenol (DON) is a common mycotoxin that contaminates cereals and their by-products. The gastrointestinal tract is the first physical barrier against ingested food contaminants. DON contributes to the loss of barrier function of the intestine through the decreased expression of claudin-4 protein, a tight junction protein. The mechanism by which DON alters the intestinal barrier function remains poorly characterized. Therefore, we investigated the involvement of mitogen-activated protein kinases (MAPK) in the DON-induced loss of barrier function. We first verified that 30 µmol/L of DON activated MAPK in a highly sensitive porcine intestinal epithelial cell line (IPEC-1). Inhibition of p44/42 extracellular signal-regulated kinase (ERK) phosphorylation, with 0.5 µmol/L of the specific MAPK pharmacological inhibitor U0126 for 2 h, restored the barrier function of the differentiated intestinal epithelial cell monolayers. The restoration of barrier function was evaluated by trans-epithelial electrical resistance measurements and tracer flux paracellular permeability experiments. The U0126 also restored the intestinal expression of claudin-4 protein, thereby demonstrating that MAPK activation is involved in claudin-4 protein expression and claudin-4 is involved in the maintenance of the intestinal epithelial cell barrier function. Further experiments indicated that p44/42 ERK is not involved in the transcriptional regulation of claudin-4. In conclusion, we demonstrated that DON-induced activation of the p44/42 ERK signaling pathway inhibits the expression of claudin-4 protein, which leads to impaired intestinal barrier function. Given the high levels of DON in cereal grains, these observations of impaired barrier function have implications for human and animal health.

Phytic acid protects porcine intestinal epithelial cells from deoxynivalenol (DON) cytotoxicity

The purpose of this study was to evaluate the effects of phytic acid (IP(6)) as a possible inhibitor of cellular damage induced by toxic substances such as mycotoxins on a porcine intestinal epithelial cell line (IPEC-1). We first observed that a dose of 5 mM phytic acid decreases cell viability and transepithelial electrical resistance (TEER) of cell monolayer. We next investigate the effect of non-cytotoxic dose of phytic acid on the deoxinivalenol (DON) induced decreased TEER. We showed that treatment with 0.5 mM or 1.0 mM phytic acid restores the decrease in TEER caused by 25 μM DON. In conclusion this study demonstrates that phytic acid decreased the negative effects of deoxynivalenol on the membrane integrity of the IPEC-1 intestinal epithelial cell line.

Clathrin-mediated endocytosis and transcytosis of enterotoxigenic Escherichia coli F4 fimbriae in porcine intestinal epithelial cells

Enterotoxigenic Escherichia coli (ETEC) cause severe diarrhea in neonatal and recently weaned piglets. Previously, we demonstrated that oral immunization of F4 receptor positive piglets with purified F4 fimbriae induces a protective F4-specific intestinal immune response. However, in F4 receptor negative animals no F4-specific immune response can be elicited, indicating that the induction of an F4-specific mucosal immune response upon oral immunisation is receptor-dependent. Although F4 fimbriae undergo transcytosis across the intestinal epithelium in vivo, the endocytosis pathways used remain unknown. In the present study, we characterized the internalization of F4 fimbriae in the porcine intestinal epithelial cell line IPEC-J2. The results in the present study demonstrate that F4 fimbriae are internalized through a clathrin-dependent pathway. Furthermore, our results suggest that F4 fimbriae are transcytosed across differentiated IPEC-J2 cells. This receptor-dependent transcytosis of F4 fimbriae may explain the immunogenicity of these fimbriae upon oral administration in vivo.

Porcine in vitro and in vivo models to assess the virulence of Salmonella enterica serovar Typhimurium for pigs

Salmonella Typhimurium infections in pigs pose an important human health hazard. One promising control measure is the development of live attenuated vaccine strains using defined knockout mutants. Preferably, screening of candidate knockout vaccine strains for attenuation should first be done in models allowing testing of a large number of strains. Thereafter, a limited number of selected strains should be further characterized in an experimental infection model in pigs. The aim of the present study was to develop such models. The invasive and proliferative characteristics of S. Typhimurium were assessed in both a non-polarized and a polarized porcine intestinal epithelial cell line. Neutrophils obtained from porcine blood were used to study the capacity of Salmonella to withstand killing by these phagocytes. The ability to induce an intestinal inflammatory response was investigated in a terminal intestinal loop model. The systemic phase of infection was mimicked by studying the uptake and intracellular survival of S. Typhimurium in porcine pulmonary alveolar macrophages and peripheral blood monocytes. These models should allow screening for attenuated strains. For further characterization, an experimental infection model was established, providing extensive data on the course of an oral infection and the optimal time points for colonization (day 5 postinoculation [pi]) and persistency (days 21-28 pi) in pigs. In conclusion, screening for virulence of S. Typhimurium strains with subsequent confirmation for a subset of strains in a well-defined experimental infection model would significantly reduce the number of experimental pigs required.

Evaluación de la citotoxicidad de la aflatoxina y la fumonisina en células intestinales de porcino

The coexistence of the aflatoxin (AFB) and fumonisin (FB) has been widely documented in many parts of the world. However, few studies describing the synergy effect of both mycotoxins in vivo and/or in vitro are available. The objective of this study consisted on evaluating the effect of AFB and FB on the morphology, the capacity of cellular proliferation, cytotoxicity and interleukin-8 (IL-8) synthesis in a porcine intestinal epithelial cell line (IPEC-1). Concerning to the cellular morphology it was only affected in the concentrations higher of AFB (50 microM) and FB (500 microM). However, the cellular proliferation, the cellular damage and synthesis of IL-8 they were affected when present in combination the AFB/FB (1.3/3.7; 2/3.7 and 5/10 microM respectively) with that showed by the individual effect of similar concentrations of these mycotoxins (p < 0.05). Our data indicate that the combination of AFB/FB in low concentrations showed a synergy effect, altering the cellular morphophysiology, which can imply in vivo the entrance of other toxins or biological agents for alteration of the intestinal barrier impacting negatively in the human or animal health.

Effects of surfactant protein D on growth, adhesion and epithelial invasion of intestinal Gram-negative bacteria

Surfactant protein D (SP-D) interacts with various different microorganisms and plays an important role in pulmonary innate immunity. SP-D expression has also been detected in extrapulmonary tissues, including the gastro-intestinal tract. However, its function in the intestine is unknown and may differ considerably from SP-D functions in the lung. Therefore, the effects of porcine SP-D (pSP-D) on several strains of intestinal bacteria were studied by means of bacterial growth assays, colony-count assays, radial diffusion assays and differential fluorescent staining. Furthermore, the effect of pSP-D on the adhesion- and invasion-characteristics was investigated. All bacterial strains tested in this study were aggregated by pSP-D, but only Escherichia coli K12 was susceptible to pSP-D-mediated growth inhibition. Bacterial membrane integrity of E. coli K12 was affected by pSP-D, but this did not lead to a reduced bacterial viability. Therefore, it is unlikely that pSP-D has a direct antimicrobial effect, and the observed effects are most likely due to pSP-D-mediated bacterial aggregation. The effects of pSP-D on bacterial adhesion and invasion were studied with the porcine intestinal epithelial cell line IPI-2I. Preincubation with pSP-D results in a several-fold increase in adhesion ( E. coli and Salmonella) and invasion ( Salmonella), but did not affect the IL-8 production induced by the bacteria. Results obtained in this study suggest that pSP-D promotes uptake of pathogenic bacteria by epithelial cells. This may reflect a scavenger function for pSP-D in the intestine, which enables the host to generate a more rapid response to infectious bacteria.

Fumonisin B 1 exposure and its selective effect on porcine jejunal segment: Sphingolipids, glycolipids and trans-epithelial passage disturbance

Fumonisin B 1 (FB 1) is a mycotoxin produced by Fusarium verticillioides, the cause of Fusarium kernel rot in maize. FB 1 is toxic in domestic and laboratory animals, including pigs. This study investigated the effects of a seven-days-exposure of 1.5 mg/kg b.w. FB 1 on the porcine intestinal epithelium. Statistically significant increases in the ratio of sphinganine to sphingosine, as well as alterations of the glycolipid distribution were observed in the jejunum. Using a porcine intestinal epithelial cell line (IPEC-1) derived from jejunum and ileum, we tested the effect of FB 1 in vitro in a time- and dose-dependent fashion. A significant increase in sphinganine concentration was observed after 2 days of FB 1 exposure at concentrations >100 μM, or from 6 days of FB 1 exposure at concentration >20 μM. We were also able to show that FB 1 exposure at 200 μM during 16 days increased the intestinal trans-epithelial flux of FB 1. These data indicate that, in pigs, this mycotoxin acts selectively on jejunum cells as follows: (i) FB 1 affects sphingolipid metabolism, as demonstrated by an increase of the amount of free sphingoid bases in a time- and dose-dependent manner, (ii) a depletion of the glycolipids in plasma membranes is observed, and (iii) an increase occurs in the trans-epithelial flux.

Detection and distribution of probiotic Escherichia coli Nissle 1917 clones in swine herds in Germany

To verify the presence of Escherichia coli Nissle 1917 as a natural isolate in swine and to characterize in vitro probiotic properties as well as in vivo persistence in a feeding experiment. During studies on the intestinal microflora of pigs, we isolated E. coli Nissle 1917 sporadically from a pig population over a period of 1 year. The identity of the isolates as E. coli Nissle 1917 was verified by serotyping, Nissle-specific PCR, macrorestriction analysis (pulsed field gel electrophoresis) and the determination of in vitro probiotic properties in invasion and adhesion assays using a porcine intestinal epithelial cell line. Both the E. coli isolates and the E. coli Nissle 1917 strain showed strong reductions in adhesion of porcine enteropathogenic E. coli and invasion of Salmonella typhimurium with epithelial cells in vitro, with a probiotic effect. Screening of five epidemiologically unlinked swine farms and two wild boar groups showed one farm positive for E. coli Nissle 1917. A feeding experiment with four piglets showed viable E. coli Nissle 1917 in the intestine of three animals. The results of this study suggest that the E. coli Nissle 1917 strain is already partially established in swine herds, but the colonization of individual animals is variable. We report natural, long-term colonization and transmission of the probiotic E. coli Nissle 1917 strain in a swine herd, characterized individual persistence and colonization properties in swine and established an in vitro porcine intestinal epithelial cell model of probiotic action. The results of this study would have implications in the use of this strain as a probiotic in swine and contribute to a better understanding of the individual nature of intestinal bacterial persistence and establishment.

Mycotoxin fumonisin B 1 selectively down-regulates the basal IL-8 expression in pig intestine: in vivo and in vitro studies

Fumonisin B 1 (FB 1) is a mycotoxin produced by Fusarium verticillioides and F. proliferatum, common contaminants of maize. FB 1 causes toxicological effects in laboratory and domestic animals including pigs. The gastrointestinal tract represents a barrier encountered by exogenous food compounds. The purpose of our study was to determine FB 1 effects on intestinal immune response. Nine recently weaned piglets orally received 0.5 mg of purified toxin/kg of body weight/day for 7 days, while eight other animals were kept as controls. After necropsy, ileal samples were analyzed for five pro-inflammatory cytokines mRNA expression by RT-PCR. No difference was observed for IL-1β, IL-6, IL-12 and TNF-β mRNA levels between control and FB 1-treated animals. In contrast, FB 1 treatment induced a significant down-regulation of the expression of IL-8 mRNA in the pig ilea. The effect of FB 1 on the IL-8 expression was also examined in the porcine intestinal epithelial cell line IPEC-1. FB 1 decreases the expression of IL-8, both at the mRNA and protein levels, in a dose-dependant manner. Taken together, our data demonstrate that FB 1 alters the intestinal immune response by decreasing the level of IL-8. This may contribute to the increased intestinal colonization by pathogenic Escherichia coli that was observed in FB 1-treated pigs and may have implications for humans/animals consuming FB 1-contaminated food/feed.

Characterization of a porcine intestinal epithelial cell line for in vitro studies of microbial pathogenesis in swine

In vitro studies on the pathogenesis in swine have been hampered by the lack of relevant porcine cell lines. Since many bacterial infections are swine-specific, studies on pathogenic mechanisms require appropriate cell lines of porcine origin. We have characterized the permanent porcine intestinal epithelial cell line, IPEC-J2, using a variety of methods in order to assess the usefulness of this cell line as an in vitro infection model. Electron microscopic analyses and histochemical staining revealed the cells to be enterocyte-like with microvilli, tight junctions and glycocalyx-bound mucin. The functional integrity of monolayers was determined by transepithelial electrical resistance (TEER) measurements. Both commensal bacteria and important bacterial pathogens were chosen for study based on their principally different infection mechanisms: obligate extracellular Escherichia coli, facultative intracellular Salmonella and obligate intracellular Chlamydia. We determined the colonization and proliferation of the bacteria on and within the host cells and monitored the host cell response. We verified the expression of mRNAs encoding the cytokines IL-1alpha, -6, -7, -8, -18, TNF-alpha and GM-CSF, but not TGF-beta or MCP-1. IL-8 protein expression was enhanced by Salmonella invasion. We conclude that the IPEC-J2 cell line provides a relevant in vitro model system for porcine intestinal pathogen-host cell interactions.

The Mycotoxin Fumonisin B1 Alters the Proliferation and the Barrier Function of Porcine Intestinal Epithelial Cells

Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium verticillioides (formerly F. moniliforme), a fungus that commonly contaminates maize. FB1 causes toxicological effects in laboratory and domestic animals including pigs. Because the gastrointestinal tract represents the first barrier met by exogenous food compounds, the purpose of this study was to investigate the effects of FB1 on IPEC-1, a porcine intestinal epithelial cell line. We first verified that low concentrations of FB1 did not exert any cytotoxic effect on IPEC-1. Indeed, significant LDH release was only observed for FB1 concentrations greater than 50 and 700 microM on proliferating and nonproliferating cells, respectively. We then demonstrated that FB1 inhibits proliferation of IPEC-1. Fluorescence-activated cell sorting (FACS) analysis of the cell cycle indicated that FB1 blocks the proliferation of intestinal cells in the G0/G1 phase. Similar results were obtained with LLC-PK1, a renal porcine epithelial cell line, which is considered to be a good model for studying FB1 in vitro effects. We have also assessed the effects of FB1 on the integrity of the barrier formed by the intestinal epithelium. We demonstrated that FB1 decreases the transepithelial electrical resistance (TEER) of IPEC-1 in a time- and dose-dependent manner. This effect was only noticed after a long exposure (8-12 days of treatment). FB1 induced the TEER decrease independently of the cell differentiation stage, and this effect was partially reversible. Taken together, our data indicate that FB1 alters the proliferation and the barrier function of intestinal cells. These results may have implications for humans and animals consuming FB1-contaminated food or feed.

PP003 Characterization of a porcine intestinal epithelial cell line for in vitro studies of microbial pathogenesis in swine

PP003 Characterization of a porcine intestinal epithelial cell line for in vitro studies of microbial pathogenesis in swine