Species Specificity of In Vitro Escherichia coli Adherence to Host Intestinal Cell Membranes and Its Correlation with In Vitro Colonization and Infectivity

1980 ◽  
Vol 28 (3) ◽  
pp. 1019-1027 ◽  
Author(s):  
Christopher P. Cheney ◽  
Peter A. Schad ◽  
Samuel B. Formal ◽  
Edgar C. Boedeker
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Guinea Pigs ◽  
Species Specificity ◽  
Intestinal Cell ◽  
Resected Specimen ◽  
Brush Borders

We have previously described an in vitro assay for examining the mucosal adherence of a rabbit diarrheagenic Escherichia coli , RDEC-1. That assay defined the in vitro characteristics of RDEC-1 adherence to brush borders isolated from rabbit ileal epithelial cells. The present study was conducted to examine the species specificity of both in vitro RDEC-1 adherence and in vivo infectivity of RDEC-1 and to compare these specificities. Species specificity in vitro adherence was examined by using brush borders prepared from intestinal epithelial cells of rats, guinea pigs, and rabbits, as well as from a surgically resected specimen of human ileum. Strain RDEC-1 adherence to rabbit brush borders in vitro was significantly greater ( P < 0.001) than its adherence to brush borders from any of the other species. Regional specificity of in vitro adherence of RDEC-1 to ileal segments of rabbit intestinal mucosa was also demonstrated. There was significantly greater adherence of RDEC-1 to rabbit ileal brush borders as compared to rabbit jejunal brush borders ( P < 0.05). In vivo infectivity was assessed by inoculating RDEC-1 into rats, guinea pigs, and rabbits. RDEC-1 elicited diarrhea in all inoculated rabbits with the mean onset of illness occurring 5 days after inoculation. In contrast, none of the RDEC-1-inoculated rats or guinea pigs developed diarrhea. Furthermore, colonization studies in these animals revealed that RDEC-1 heavily colonized the ileum and cecum (10 9 RDEC-1 colony-forming units/g of tissue) of rabbits; however, only minimal colonization was observed in guinea pigs and rats. In conclusion, the correlation between in vitro adherence and in vivo infectivity that we have observed suggests that the presence of receptors, specific for bacteria, on the surface of the host intestinal mucosa determines species susceptibility to enteric colonization and infectivity by certain strains of enteropathogenic E. coli .

scholarly journals Contributions of O Island 48 to Adherence of Enterohemorrhagic Escherichia coli O157:H7 to Epithelial Cells In Vitro and in Ligated Pig Ileal Loops

2009 ◽  
Vol 75 (18) ◽  
pp. 5779-5786 ◽  
Author(s):  
Xianhua Yin ◽  
Roger Wheatcroft ◽  
James R. Chambers ◽  
Bianfang Liu ◽  
Jing Zhu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Cluster Formation ◽  
Gene Clusters ◽  
Enterohemorrhagic Escherichia Coli ◽  
Wild Type ◽  
The Difference ◽  
Large Clusters

ABSTRACT O island 48 (OI-48) of Escherichia coli consists of three functional gene clusters that encode urease, tellurite resistance (Ter), and putative adhesins Iha and AIDA-1. The functions of these clusters in enterohemorrhagic E. coli (EHEC) O157:H7 infection are unknown. Deletion mutants for these three regions were constructed and evaluated for their ability to adhere to epithelial cells in vitro and in ligated pig ileal loops. Deletion of the Ter gene cluster reduced the ability of the organism to adhere to and form large clusters on IPEC-J2 and HEp-2 cells. Complementation of the mutation by introducing the wild-type ter genes restored adherence and large-cluster formation. Tests in ligated pig ileal loops showed a decrease in colonization by the Ter-negative mutant, but the difference was not significant compared to colonization by the wild type (26.4% ± 21.2% versus 40.1% ± 19.1%; P = 0.168). The OI-48 aidA gene deletion had no effect on adherence in vitro or in vivo. Deletion of the iha and ureC genes had no effect on adherence in vitro but significantly reduced the colonization of EHEC O157:H7 in the ligated pig intestine. These data suggest that Ter, Iha, and urease may contribute to EHEC O157:H7 pathogenesis by promoting adherence of the pathogen to the host intestinal epithelium.

scholarly journals Bactofection of lung epithelial cells in vitro and in vivo using a genetically modified Escherichia coli

Gene Therapy ◽  
2008 ◽  
Vol 15 (6) ◽  
pp. 434-442 ◽  
Author(s):  
M D B Larsen ◽  
U Griesenbach ◽  
S Goussard ◽  
D C Gruenert ◽  
D M Geddes ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Genetically Modified ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Prolonged NF-κB Activation by a Macrophage Inhibitory Cytokine 1-Linked Signal in Enteropathogenic Escherichia coli-Infected Epithelial Cells

2013 ◽  
Vol 81 (6) ◽  
pp. 1860-1869 ◽  
Author(s):  
Hye Jin Choi ◽  
Juil Kim ◽  
Kee Hun Do ◽  
Seong-Hwan Park ◽  
Yuseok Moon
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Watery Diarrhea ◽  
Intestinal Epithelial ◽  
Severe Injuries ◽  
Epithelial Integrity ◽  
Content Type

ABSTRACTIntestinal epithelial activation of nuclear factor kappa B (NF-κB) exerts both detrimental and beneficial functions in response to various luminal insults, including ones associated with mucosa-associated pathogens. Gastrointestinal infection with enteropathogenicEscherichia coli(EPEC) causes severe injuries in epithelial integrity and leads to watery diarrhea. The present study was conducted to investigate the prolonged epithelial responses to persistent EPEC infection via NF-κB activation. EPEC infection led to sustained activation of NF-κB signal in mouse intestinal epithelial cellsin vivoandin vitro, which was positively associated with a type III secretion system, whereas early NF-κB is regulated. Moreover, prolonged NF-κB activation was found to be a part of macrophage inhibitory cytokine 1 (MIC-1)-mediated signaling activation, a novel link between NF-κB signaling and infection-associated epithelial stress. EPEC infection induced gene expression of MIC-1, a member of the transforming growth factor β (TGF-β) superfamily, which then activated TGF-β-activated kinase 1 and consequently led to NF-κB activation. Functionally, both EPEC-induced MIC-1 and NF-κB signaling mediated epithelial survival by enhancing the expression of cyclin D1, a target of NF-κB. In summary, the results of the present study suggest that MIC-1 serves as a mediator of prolonged NF-κB activation, which is critical in maintaining gut epithelial integrity in response to infection-induced injuries.

scholarly journals Bacterial Lysis Liberates the Neutrophil Migration Suppressor YbcL from the Periplasm of Uropathogenic Escherichia coli

2014 ◽  
Vol 82 (12) ◽  
pp. 4921-4930 ◽  
Author(s):  
Megan E. Lau ◽  
Elizabeth S. Danka ◽  
Kristin M. Tiemann ◽  
David A. Hunstad
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Epithelial Cells ◽  
Neutrophil Migration ◽  
Outer Membrane Vesicles ◽  
Bacterial Invasion ◽  
Bladder Epithelium ◽  
Content Type

ABSTRACTUropathogenicEscherichia coli(UPEC) modulates aspects of the innate immune response during urinary tract infection to facilitate bacterial invasion of the bladder epithelium, a requirement for the propagation of infection. For example, UPEC-encoded YbcL suppresses the traversal of bladder epithelia by neutrophils in both anin vitromodel and anin vivomurine cystitis model. The suppressive activity of YbcL requires liberation from the bacterial periplasm, though the mechanism of release is undefined. Here we present findings on the site of action of YbcL and demonstrate a novel mode of secretion for a UPEC exoprotein. Suppression of neutrophil migration by purified YbcLUTI, encoded by cystitis isolate UTI89, required the presence of a uroepithelial layer; YbcLUTIdid not inhibit neutrophil chemotaxis directly. YbcLUTIwas released to a greater extent during UPEC infection of uroepithelial cells than during that of neutrophils. Release of YbcLUTIwas maximal when UPEC and bladder epithelial cells were in close proximity. Established modes of secretion, including outer membrane vesicles, the type II secretion system, and the type IV pilus, were dispensable for YbcLUTIrelease from UPEC. Instead, YbcLUTIwas liberated during bacterial death, which was augmented upon exposure to bladder epithelial cells, as confirmed by detection of bacterial cytoplasmic proteins and DNA in the supernatant and enumeration of bacteria with compromised membranes. As YbcLUTIacts on the uroepithelium to attenuate neutrophil migration, this mode of release may represent a type of altruistic cooperation within a UPEC population during colonization of the urinary tract.

scholarly journals The Afa/Dr Adhesins of Diffusely Adhering Escherichia coli Stimulate Interleukin-8 Secretion, Activate Mitogen-Activated Protein Kinases, and Promote Polymorphonuclear Transepithelial Migration in T84 Polarized Epithelial Cells

2003 ◽  
Vol 71 (3) ◽  
pp. 1068-1074 ◽  
Author(s):  
Fréderic Bétis ◽  
Patrick Brest ◽  
Véronique Hofman ◽  
Julie Guignot ◽  
Marie-Françoise Bernet-Camard ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Protein Kinases ◽  
Interleukin 8 ◽  
Intestinal Cell ◽  
Proinflammatory Response ◽  
T84 Cells ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

ABSTRACT Afa/Dr diffusely adhering Escherichia coli (Afa/Dr DAEC) strains cause symptomatic urinary tract and intestinal infections. The proinflammatory effects of Afa/Dr DAEC strains in vitro have been not investigated to date. In the present study, we used confluent polarized monolayers of intestinal cell line T84 to evaluate the consequences of epithelial infection by Afa/Dr DAEC strains in terms of proinflammatory response. Polymorphonuclear leukocyte (PMNL) migration across the epithelial barrier was induced after incubation of the T84 monolayers with the wild-type Afa/Dr DAEC strain C1845 harboring the fimbrial F1845 adhesin and strain IH11128 harboring the Dr hemagglutinin, and the E. coli laboratory strain HB101 was transformed with the pSSS1 plasmid, producing Afa/Dr F1845 adhesin. PMNL migrations were correlated with a basolateral secretion of interleukin-8 by T84 cells and were abolished after incubation of epithelial cells with an anti-decay accelerating factor (DAF) antibody that recognized the short consensus repeat 3 domain of DAF (monoclonal antibody 1H4). Moreover, Afa/Dr DAEC strains induced tyrosine phosphorylation of several T84 proteins and activated the mitogen-activated protein kinases (ERK1/2 mitogen-activated protein, P38, and Jun-C kinases). These data demonstrated for the first time that, in vitro, Afa/Dr DAEC strains exert a proinflammatory signal in intestinal epithelial cells.

scholarly journals Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Cheng-Rung Huang ◽  
Cheng-Ju Kuo ◽  
Chih-Wen Huang ◽  
Yu-Ting Chen ◽  
Bang-Yu Liu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Enterohemorrhagic Escherichia Coli ◽  
Intestinal Cell ◽  
Intestinal Cells ◽  
Cyclin Dependent Kinase ◽  
C Elegans ◽  
Mitotic Cyclin ◽  
Human Intestinal Cells

AbstractEnterohemorrhagic Escherichia coli (EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a Caenorhabditis elegans model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of C. elegans as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement.

scholarly journals 699. Bactofection into Airway Epithelial Cells In Vitro and In Vivo Using a Genetically Modified Escherichia coli

2006 ◽  
Vol 13 ◽  
pp. S270-S271
Author(s):  
Mia D.B. Larsen ◽  
Uta Griesenbach ◽  
Sylvie Goussard ◽  
Dieter Gruenert ◽  
Duncan M. Geddes ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Genetically Modified ◽  
Airway Epithelial Cells ◽  
Airway Epithelial

Secreted adhesion molecules of Strongyloides venezuelensis are produced by oesophageal glands and are components of the wall of tunnels constructed by adult worms in the host intestinal mucosa

Parasitology ◽  
2003 ◽  
Vol 126 (2) ◽  
pp. 165-171 ◽  
Author(s):  
H. MARUYAMA ◽  
M. EL-MALKY ◽  
T. KUMAGAI ◽  
N. OHTA
Keyword(s):  
Epithelial Cells ◽  
Adhesion Molecules ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Parasitic Female ◽  
Strongyloides Venezuelensis ◽  
Infection Processes

The parasitic female of Strongyloides venezuelensis keeps invading the epithelial layer of the host intestinal mucosa. Upon invasion, it adheres to the surface of the intestinal epithelial cells with adhesion molecules secreted from the mouth. It has been demonstrated that S. venezuelensis are expelled from the intestine because mucosal mast cells inhibit the attachment of adult worms to the mucosal surface. In the present study, we generated specific antibodies against secreted adhesion molecules to investigate their function in vivo, because these molecules have been demonstrated only in vitro in spite of the importance in the infection processes. A mouse monoclonal antibody specific to S. venezuelensis adhesion molecules inhibited the attachment of adult worms to plastic dishes and the binding of adhesion molecules to rat intestinal epithelial cells. Immunohistochemical study revealed that adhesion molecules were produced by oesophageal glands and were continuously secreted in vivo to line the wall of the tunnels formed by adult worms in the intestinal mucosa. Our findings indicate that adhesion molecules play essential roles in the infection processes of S. venezuelensis in the host intestine.

scholarly journals Mycobacterium avium Infection of Epithelial Cells Results in Inhibition or Delay in the Release of Interleukin-8 and RANTES

1999 ◽  
Vol 67 (10) ◽  
pp. 5069-5075 ◽  
Author(s):  
Felix J. Sangari ◽  
Mary Petrofsky ◽  
Luiz E. Bermudez
Keyword(s):  
Epithelial Cells ◽  
Mycobacterium Avium ◽  
Intestinal Mucosa ◽  
Inflammatory Cells ◽  
Interleukin 8 ◽  
Cell Culture Supernatant ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ht 29

ABSTRACT Mycobacterium avium is an opportunistic pathogen in AIDS patients, who acquire the infection mainly through the gastrointestinal tract. Previous studies in vitro have shown thatM. avium invades epithelial cells of both intestinal and laryngeal origin. In addition, M. avium enters the intestinal mucosa of healthy mice. Because M. aviuminvasion of the intestinal mucosa in vivo initially is not accompanied by significant influx of inflammatory cells, we sought to determine whether M. avium would trigger chemokine release upon entry into epithelial cells by using HT-29 intestinal and HEp-2 laryngeal epithelial cell lines. Chemokine synthesis was measured both by the presence of specific mRNA and protein secretion in the cell culture supernatant as determined by enzyme-linked immunosorbent assay. Infection of HT-29 intestinal cells with M. avium did not induce the release of interleukin-8 (IL-8) or RANTES for up to 7 days postinfection. However, infection of HEp-2 cells resulted in the release of IL-8 and RANTES at 72 h. Similar findings were observed with other AIDS M. avium isolates belonging to different serovars. Secretion of IL-8 by HEp-2 cells was dependent upon bacterial uptake. In addition, prior infection with M. aviumsuppressed IL-8 production by HT-29 cells infected withSalmonella typhimurium. Our results suggest that M. avium infection of epithelial cells is associated with a delay in IL-8 and RANTES production which, in the case of HT-29, is prolonged up to 1 week. These findings may explain the weak inflammatory response after intestinal mucosa invasion in mice and are probably related with the ability of the bacterium to evade the host’s immune response.

Sign in / Sign up

Export Citation Format

Share Document