Biogenic Polyphosphate Nanoparticles fromSynechococcussp. PCC 7002 Exhibit Intestinal Protective Potential in Human Intestinal Epithelial Cells In Vitro and Murine Small Intestine Ex Vivo

2018 ◽  
Vol 66 (30) ◽  
pp. 8026-8035 ◽  
Author(s):  
Guangxin Feng ◽  
Yinong Feng ◽  
Tengjiao Guo ◽  
Yisheng Yang ◽  
Wei Guo ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Ex Vivo ◽  
Intestinal Epithelial ◽  
Protective Potential ◽  
Human Intestinal Epithelial Cells ◽  
Murine Small Intestine

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.

Suppressor of cytokine signaling-2 limits intestinal growth and enterotrophic actions of IGF-I in vivo

2006 ◽  
Vol 291 (3) ◽  
pp. G472-G481 ◽  
Author(s):  
Carmen Z. Michaylira ◽  
James G. Simmons ◽  
Nicole M. Ramocki ◽  
Brooks P. Scull ◽  
Kirk K. McNaughton ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Ex Vivo ◽  
Cytokine Signaling ◽  
Intestinal Epithelial ◽  
Growth Responses ◽  
Intestinal Growth ◽  
Igf I

Suppressors of cytokine signaling (SOCS) typically limit cytokine receptor signaling via the JAK-STAT pathway. Considerable evidence demonstrates that SOCS2 limits growth hormone (GH) action on body and organ growth. Biochemical evidence that SOCS2 binds to the IGF-I receptor (IGF-IR) supports the novel possibility that SOCS2 limits IGF-I action. The current study tested the hypothesis that SOCS2 normally limits basal or IGF-I-induced intestinal growth and limits IGF-IR signaling in intestinal epithelial cells. Intestinal growth was assessed in mice homozygous for SOCS2 gene deletion (SOCS2 null) and wild-type (WT) littermates at different ages and in response to infused IGF-I or vehicle or EGF and vehicle. The effects of SOCS2 on IGF-IR signaling were examined in ex vivo cultures of SOCS2 null and WT intestine and Caco-2 cells. Compared with WT, SOCS2 null mice showed significantly enhanced small intestine and colon growth, mucosal mass, and crypt cell proliferation and decreases in radiation-induced crypt apoptosis in jejunum. SOCS2 null mice showed significantly greater growth responses to IGF-I in small intestine and colon. IGF-I-stimulated activation of IGF-IR and downstream signaling intermediates were enhanced in the intestine of SOCS2 null mice and were decreased by SOCS2 overexpression in Caco-2 cells. SOCS2 bound directly to the endogenous IGF-IR in Caco-2 cells. The intestine of SOCS2 null mice also showed enhanced growth responses to infused EGF. We conclude that SOCS2 normally limits basal and IGF-I- and EGF-induced intestinal growth in vivo and has novel inhibitory effects on the IGF-IR tyrosine kinase pathway in intestinal epithelial cells.

scholarly journals Carrageenan Induces Cell Cycle Arrest in Human Intestinal Epithelial Cells in Vitro

2008 ◽  
Vol 138 (3) ◽  
pp. 469-475 ◽  
Author(s):  
Sumit Bhattacharyya ◽  
Alip Borthakur ◽  
Pradeep K. Dudeja ◽  
Joanne K. Tobacman
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Cell Cycle Arrest ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Cycle Arrest ◽  
Human Intestinal Epithelial Cells

scholarly journals The influence of microbial metabolites on human intestinal epithelial cells and macrophages in vitro

2005 ◽  
Vol 45 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Marleen H.M.C. Nuenen ◽  
Rianne A.F. Ligt ◽  
Robert P. Doornbos ◽  
Janneke C.J. Woude ◽  
Ernst J. Kuipers ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Microbial Metabolites ◽  
Human Intestinal Epithelial Cells

scholarly journals Expression of Human Decay-Accelerating Factor on Intestinal Epithelium of Transgenic Mice Does Not Facilitate Infection by the Enteral Route

2015 ◽  
Vol 89 (8) ◽  
pp. 4311-4318 ◽  
Author(s):  
Jieyan Pan ◽  
Lili Zhang ◽  
Matthew A. Odenwald ◽  
Le Shen ◽  
Jerrold R. Turner ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transgenic Mice ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cells ◽  
Apical Cell ◽  
Oral Route ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cells ◽  
Cvb3 Infection

ABSTRACTIn vitro, infection of polarized human intestinal epithelial cells by coxsackievirus B3 (CVB3) depends on virus interaction with decay-accelerating factor (DAF), a receptor expressed on the apical cell surface. Although mice are highly susceptible to CVB3 infection when virus is delivered by intraperitoneal injection, infection by the enteral route is very inefficient. Murine DAF, unlike human DAF, does not bind virus, and we hypothesized that the absence of an accessible receptor on the intestinal surface is an important barrier to infection by the oral route. We generated transgenic mice that express human DAF specifically on intestinal epithelium and measured their susceptibility to infection by a DAF-binding CVB3 isolate. Human DAF permitted CVB3 to bind to the intestinal surfaceex vivoand to infect polarized monolayers of small-intestinal epithelial cells derived from DAF transgenic mice. However, expression of human DAF did not facilitate infection by the enteral route either in immunocompetent animals or in animals deficient in the interferon alpha/beta receptor. These results indicate that the absence of an apical receptor on intestinal epithelium is not the major barrier to infection of mice by the oral route.IMPORTANCECVB3 infection of human intestinal epithelial cells depends on DAF at the apical cell surface, and expression of human DAF on murine intestinal epithelial cells permits their infectionin vitro. However, expression of human DAF on the intestinal surface of transgenic mice did not facilitate infection by the oral route. Although the role of intestinal DAF in human infection has not been directly examined, these results suggest that DAF is not the critical factor in mice.

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