scholarly journals Comparative Transcriptome Profiling of Human and Pig Intestinal Epithelial Cells after Porcine Deltacoronavirus Infection

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 292
Author(s):  
Diana Cruz-Pulido ◽  
Patricia A. Boley ◽  
Wilberforce Zachary Ouma ◽  
Moyasar A. Alhamo ◽  
Linda J. Saif ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Intestinal Epithelial Cells ◽  
Expression Profiles ◽  
Human Cells ◽  
Host Cells ◽  
Transcriptional Level ◽  
Intestinal Epithelial

Porcine deltacoronavirus (PDCoV) is an emerging infectious disease of swine with zoonotic potential. Phylogenetic analysis suggests that PDCoV originated recently from a host-switching event between birds and mammals. Little is known about how PDCoV interacts with its differing hosts. Human-derived cell lines are susceptible to PDCoV infection. Herein, we compare the gene expression profiles of an established host swine cells to potential emerging host human cells after infection with PDCoV. Cell lines derived from intestinal lineages were used to reproduce the primary sites of viral infection in the host. Porcine intestinal epithelial cells (IPEC-J2) and human intestinal epithelial cells (HIEC) were infected with PDCoV. RNA-sequencing was performed on total RNA extracted from infected cells. Human cells exhibited a more pronounced response to PDCoV infection in comparison to porcine cells with more differentially expressed genes (DEGs) in human, 7486, in comparison to pig cells, 1134. On the transcriptional level, the adoptive host human cells exhibited more DEGs in response to PDCoV infection in comparison to the primary pig host cells, where different types of cytokines can control PDCoV replication and virus production. Key immune-associated DEGs and signaling pathways are shared between human and pig cells during PDCoV infection. These included genes related to the NF-kappa-B transcription factor family, the interferon (IFN) family, the protein-kinase family, and signaling pathways such as the apoptosis signaling pathway, JAK-STAT signaling pathway, inflammation/cytokine–cytokine receptor signaling pathway. MAP4K4 was unique in up-regulated DEGs in humans in the apoptosis signaling pathway. While similarities exist between human and pig cells in many pathways, our research suggests that the adaptation of PDCoV to the porcine host required the ability to down-regulate many response pathways including the interferon pathway. Our findings provide an important foundation that contributes to an understanding of the mechanisms of PDCoV infection across different hosts. To our knowledge, this is the first report of transcriptome analysis of human cells infected by PDCoV.

OmpD but not OmpC is involved in adherence ofSalmonella entericaserovar Typhimurium to human cells

2004 ◽  
Vol 50 (9) ◽  
pp. 719-727 ◽  
Author(s):  
Bochiwe Hara-Kaonga ◽  
Thomas G Pistole
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Human Cells ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Wild Type ◽  
Human Macrophages ◽  
Significant Difference ◽  
Serovar Typhimurium

Conflicting reports exist regarding the role of porins OmpC and OmpD in infections due to Salmonella enterica serovar Typhimurium. This study investigated the role of these porins in bacterial adherence to human macrophages and intestinal epithelial cells. ompC and ompD mutant strains were created by transposon mutagenesis using P22-mediated transduction of Tn10 and Tn5 insertions, respectively, into wild-type strain 14028. Fluorescein-labeled wild-type and mutant bacteria were incubated with host cells at various bacteria to cell ratios for 1 h at 37 °C and analyzed by flow cytometry. The mean fluorescence intensity of cells with associated wild-type and mutant bacteria was used to estimate the number of bacteria bound per host cell. Adherence was also measured by fluorescence microscopy. Neither assay showed a significant difference in binding of the ompC mutant and wild-type strains to the human cells. In contrast, the ompD mutant exhibited lowered binding to both cell types. Our findings suggest that OmpD but not OmpC is involved in the recognition of Salmonella serovar Typhimurium by human macrophages and intestinal epithelial cells.Key words: Salmonella, adherence, porins, intestinal epithelial cells, macrophage.

scholarly journals The Enteropathogenic Escherichia coli-Secreted Protein EspZ Inhibits Host Cell Apoptosis

2012 ◽  
Vol 80 (11) ◽  
pp. 3850-3857 ◽  
Author(s):  
Jennifer Lising Roxas ◽  
John Scott Wilbur ◽  
Xiangfeng Zhang ◽  
Giovanna Martinez ◽  
Gayatri Vedantam ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Host Cell ◽  
Signaling Pathways ◽  
Intestinal Epithelial Cells ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Apoptotic Pathway ◽  
Host Signaling ◽  
Infected Cells

ABSTRACTThe diarrheagenic pathogen enteropathogenicEscherichia coli(EPEC) limits the death of infected enterocytes early in infection. A number of bacterial molecules and host signaling pathways contribute to the enhanced survival of EPEC-infected host cells. EspZ, a type III secreted effector protein that is unique to EPEC and related “attaching and effacing” (A/E) pathogens, plays a role in limiting host cell death, but the precise host signaling pathways responsible for this phenotype are not known. We hypothesized that EspZ contributes to the survival of infected intestinal epithelial cells by interfering with apoptosis. Consistent with previous studies, scanning electron microscopy analysis of intestinal epithelial cells infected with an EPECespZmutant (ΔespZ) showed increased levels of apoptotic and necrotic cells compared to cells infected with the isogenic parent strain. Correspondingly, higher levels of cytosolic cytochromecand increased activation of caspases 9, 7, and 3 were observed for ΔespZstrain-infected cells compared to wild-type (WT) EPEC-infected cells. Finally,espZ-transfected epithelial cells were significantly protected from staurosporine-induced, but not tumor necrosis factor alpha (TNF-α)/cycloheximide-induced, apoptosis. Thus, EspZ contributes to epithelial cell survival by mechanisms that include the inhibition of the intrinsic apoptotic pathway. The enhanced survival of infected enterocytes by molecules such as EspZ likely plays a key role in optimal colonization by A/E pathogens.

scholarly journals Spirulina Crude Protein Promotes the Migration and Proliferation in IEC-6 Cells by Activating EGFR/MAPK Signaling Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 205
Author(s):  
Su-Jin Jeong ◽  
Jeong-Wook Choi ◽  
Min-Kyeong Lee ◽  
Youn-Hee Choi ◽  
Taek-Jeong Nam
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Crude Protein ◽  
Cell Cycle Progression ◽  
Intestinal Epithelial Cells ◽  
Mapk Signaling ◽  
S Phase ◽  
Intestinal Epithelial ◽  
Cycle Progression

Spirulina is a type of filamentous blue-green microalgae known to be rich in nutrients and to have pharmacological effects, but the effect of spirulina on the small intestine epithelium is not well understood. Therefore, this study aims to investigate the proliferative effects of spirulina crude protein (SPCP) on a rat intestinal epithelial cells IEC-6 to elucidate the mechanisms underlying its effect. First, the results of wound-healing and cell viability assays demonstrated that SPCP promoted migration and proliferation in a dose-dependent manner. Subsequently, when the mechanisms of migration and proliferation promotion by SPCP were confirmed, we found that the epidermal growth factor receptor (EGFR) and mitogen-activated protein (MAPK) signaling pathways were activated by phosphorylation. Cell cycle progression from G0/G1 to S phase was also promoted by SPCP through upregulation of the expression levels of cyclins and cyclin-dependent kinases (Cdks), which regulate cell cycle progression to the S phase. Meanwhile, the expression of cyclin-dependent kinase inhibitors (CKIs), such as p21 and p27, decreased with SPCP. In conclusion, our results indicate that activation of EGFR and its downstream signaling pathway by SPCP treatment regulates cell cycle progression. Therefore, these results contribute to the research on the molecular mechanism for SPCP promoting the migration and proliferation of rat intestinal epithelial cells.

Tu1402 All-Trans Retinoic Acid (ATRA) Stimulates SLC26A3 Activity in Intestinal Epithelial Cells via a PI3K Signaling Pathway

2015 ◽  
Vol 148 (4) ◽  
pp. S-880 ◽  
Author(s):  
Shubha Priyamvada ◽  
Arivarasu Natarajan Anbazhagan ◽  
Anoop Kumar ◽  
Tarunmeet Gujral ◽  
Alip Borthakur ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Intestinal Epithelial Cells ◽  
Pi3k Signaling ◽  
Intestinal Epithelial ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Pi3k Signaling Pathway

Na(+)-K(+)-ATPase gene expression in rat intestine and Caco-2 cells: response to thyroid hormone

1993 ◽  
Vol 265 (4) ◽  
pp. G775-G782 ◽  
Author(s):  
R. A. Giannella ◽  
J. Orlowski ◽  
M. L. Jump ◽  
J. B. Lingrel
Keyword(s):  
Thyroid Hormone ◽  
Epithelial Cells ◽  
Enzymatic Activity ◽  
Intestinal Epithelial Cells ◽  
Blot Hybridization ◽  
Intestinal Cell ◽  
Transcriptional Level ◽  
Intestinal Epithelial ◽  
Subunit Mrna ◽  
Atpase Gene

Expression of the Na(+)-K(+)-adenosinetriphosphatase (ATPase) gene family in rat intestinal epithelial cells was examined using RNA blot hybridization analyses. Rat intestinal epithelial cells express only the alpha 1- and beta 1-subunit mRNAs. A gradient in expression of alpha 1- and beta 1-subunit mRNA was seen along the villus-crypt unit in both jejunum and ileum, i.e., villus tip >> crypt cells. Regional differences in expression were observed along the intestine. alpha 1- and beta 1-subunit mRNA abundance was similar in jejunum, ileum, and colon while enzymatic activity was highest in the jejunum and lowest in the ileum. Administration of thyroid hormone to thyroidectomized rats increased the expression of alpha 1- and beta 1-subunit mRNAs in jejunum but not in colon. Hypothyroidism had no effect on subunit mRNA expression. The human intestinal cell line Caco-2 was also studied. These cells also expressed only the alpha 1- and beta 1-isoform mRNAs and demonstrated a developmental profile in both mRNA and enzymatic activity. Furthermore, in Caco-2 cells both alpha 1- and beta 1-mRNAs and Na(+)-K(+)-ATPase enzymatic activity were stimulated by thyroid hormone. Caco-2 cells transfected with 5' flanking regions of the human Na(+)-K(+)-ATPase beta 1-gene linked to the chloramphenicol acetyltransferase (CAT) reporter gene responded to 3,5,3'-triiodothyronine (T3) treatment with increased expression of CAT activity. This suggests that the 5' flanking region of the beta 1-gene contains a thyroid hormone response element and that T3 upregulation occurs at the transcriptional level.(ABSTRACT TRUNCATED AT 250 WORDS)

Induction of endothelin-1 synthesis by IL-2 and its modulation of rat intestinal epithelial cell growth

1998 ◽  
Vol 275 (3) ◽  
pp. G556-G563 ◽  
Author(s):  
Takeharu Shigematsu ◽  
Soichiro Miura ◽  
Masahiko Hirokawa ◽  
Ryota Hokari ◽  
Hajime Higuchi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Proliferative Response ◽  
Intestinal Epithelial Cell ◽  
Culture Media ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Endothelin (ET), a vasoconstrictive peptide, is known to have a variety of biological actions. Although ET is released by vascular endothelial cells, other cell populations also have been reported to synthesize and release ET. In this study, we examined whether ET is synthesized by intestinal epithelial cells and whether it affects induction of epithelial cell proliferation by interleukin-2 (IL-2). Subconfluent monolayers of intestinal epithelial cells (IEC-6 and IEC-18) were maintained in serum-free medium before addition of rat IL-2. Both IEC-6 and IEC-18 cells released ET-1 into the medium under unstimulated conditions, as determined by a sandwich ELISA. IL-2 significantly enhanced ET-1 release in a time-dependent manner. ET-3 was not detectable in the culture media of either cell line. Expression of ET-1 and ET-3 mRNA in epithelial cells was assessed by competitive PCR. Both cell lines were shown to express ET-1 mRNA, but no ET-3 mRNA was detected. IL-2 treatment enhanced ET-1 mRNA expression by both IEC-6 and IEC-18 cells. Both cell lines also expressed mRNA for ETA and ETB receptor subtypes. When cell proliferation was assessed, exogenous ET-1 induced a slight proliferative response in both types of cells that was consistent and significant at low ET-1 concentrations; cell growth was inhibited at a higher concentration (10−7M). IL-2 produced a significant proliferative response in both cell lines. However, the addition of ET-1 (10−7 M) to culture media attenuated the IL-2-induced increase in cell proliferation. ETA-receptor antagonists significantly enhanced cellular proliferation, suggesting involvement of the ETA receptor in modulation of IL-2-induced intestinal epithelial cell growth.

Efficacy of Plant-Derived Antimicrobials in Controlling Enterohemorrhagic Escherichia coli Virulence In Vitro

2016 ◽  
Vol 79 (11) ◽  
pp. 1965-1970 ◽  
Author(s):  
SANGEETHA ANANDA BASKARAN ◽  
ANUP KOLLANOOR-JOHNY ◽  
MEERA SURENDRAN NAIR ◽  
KUMAR VENKITANARAYANAN
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Antimicrobial Agents ◽  
Intestinal Epithelial Cells ◽  
Enterohemorrhagic Escherichia Coli ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
Virulence Gene Expression ◽  
Human Intestinal Epithelial Cells

ABSTRACTEscherichia coli O157:H7 is a major foodborne pathogen that can cause serious human illness characterized by hemorrhagic diarrhea and kidney failure. The pathology of enterohemorrhagic E. coli O157:H7 (EHEC) infection is primarily mediated by verotoxins, which bind to the globotriaosylceramide receptor on host cells. Antibiotics are contraindicated for treating EHEC infection because they lead to increased verotoxin release, thereby increasing the risk of renal failure and death in patients. Thus, alternative strategies are needed for controlling EHEC infections in humans. This study investigated the effect of subinhibitory concentrations of five plant-derived antimicrobial agents (PDAs) that are generally considered as safe, i.e., trans-cinnamaldehyde, eugenol, carvacrol, thymol, and β-resorcylic acid, on EHEC motility, adhesion to human intestinal epithelial cells, verotoxin production, and virulence gene expression. All tested PDAs reduced EHEC motility and attachment to human intestinal epithelial cells (P < 0.05) and decreased verotoxin synthesis by EHEC. The reverse transcription real-time PCR data revealed that PDAs decreased the expression of critical virulence genes in EHEC (P < 0.05). The results collectively suggest that these PDAs could be used to reduce EHEC virulence, but follow-up studies in animal models are necessary to validate these findings.

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