The Campylobacter jejuni general glycosylation system is important for attachment to human epithelial cells and in the colonization of chicks

Microbiology ◽  
2004 ◽  
Vol 150 (6) ◽  
pp. 1957-1964 ◽  
Author(s):  
A. V. Karlyshev ◽  
P. Everest ◽  
D. Linton ◽  
S. Cawthraw ◽  
D. G. Newell ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Campylobacter Jejuni ◽  
Host Cells ◽  
High Similarity ◽  
Human Epithelial Cells

It has recently been shown that the enteropathogen Campylobacter jejuni has an N-linked general protein glycosylation pathway (Pgl) that modifies many of the organism's proteins. To determine the role of the N-linked general glycosylation in C jejuni, the authors studied the pglH gene, which shows high similarity to a family of sugar transferases. pglH mutants were constructed in strains 81116 and 11168H. Both mutants were shown to be deficient in their ability to glycosylate a number of C. jejuni proteins, but their lipooligosaccharide and capsule were unaffected. The pglH mutants had significantly reduced ability to adhere to and invade human epithelial Caco-2 cells. Additionally, the 81116 pglH mutant was severely affected in its ability to colonize chicks. These results suggest that glycosylation is important for the attachment of C. jejuni to human and chicken host cells and imply a role for glycoproteins in the pathogenesis of C. jejuni.

scholarly journals Apoptotic Response of Chang Cells to Infection with Pseudomonas aeruginosa Strains PAK and PAO-I: Molecular Ordering of the Apoptosis Signaling Cascade and Role of Type IV Pili

2003 ◽  
Vol 71 (5) ◽  
pp. 2665-2673 ◽  
Author(s):  
Verena Jendrossek ◽  
Sophie Fillon ◽  
Claus Belka ◽  
Ilka Müller ◽  
Beatrice Puttkammer ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Host Cells ◽  
Caspase 8 ◽  
Mitochondrial Alterations ◽  
Human Epithelial Cells ◽  
Molecular Ordering ◽  
Induced Apoptosis ◽  
Chang Cells

ABSTRACT Pseudomonas aeruginosa is a gram-negative facultative opportunistic pathogen associated with severe infections in immunocompromised hosts and in patients with cystic fibrosis. P. aeruginosa strains show divergent pathogenicity in vivo and trigger apoptosis of and/or are internalized into human host cells. In the present study, we studied the molecular ordering of apoptosis signaling upon infection of human conjunctiva epithelial Chang cells with P. aeruginosa PAK as well as the role of bacterial pili in the response to the infection. Our results show that CD95 up-regulation is followed by early activation of caspase-8 and -3 and cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase. The data also demonstrate release of apoptosis inducing factor into the cytosol of infected cells. Induction of mitochondrial alterations, i.e., mitochondrial depolarization and release of cytochrome c, as well as cleavage of caspase-9, -7, and -1 occurred only at later time points. In addition, our results demonstrate that pili are required for P. aeruginosa-induced apoptosis of human epithelial cells. While the two piliated P. aeruginosa strains, PAO-I and PAK, induced apoptosis of Chang cells within 3 h of infection, the pilus-deficient P. aeruginosa mutants PAKΔpilA and PAKΔpilAΔall were without effect. The pilus-deficient mutants failed to induce a significant up-regulation of CD95 on the cell surface and to trigger mitochondrial alterations or activation of caspase-8, -3, and -7. In addition, only the piliated wild-type strains induced caspase-1-mediated activation of interleukin-1β. Thus, pili are necessary for distinct infection-induced cellular responses of human epithelial cells.

scholarly journals Role of the Campylobacter jejuni Cj1461 DNA Methyltransferase in Regulating Virulence Characteristics

2008 ◽  
Vol 190 (19) ◽  
pp. 6524-6529 ◽  
Author(s):  
Joo-Sung Kim ◽  
Jiaqi Li ◽  
If H. A. Barnes ◽  
David A. Baltzegar ◽  
Mohanasundari Pajaniappan ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Mutant Strain ◽  
Campylobacter Jejuni ◽  
Dna Methyltransferase ◽  
Wild Type ◽  
Less Invasive ◽  
Human Epithelial Cells ◽  
Methyltransferase Gene

ABSTRACT Mutation of the cj1461 predicted methyltransferase gene reduced the motility of Campylobacter jejuni 81-176. Electron microscopy revealed that the mutant strain had flagella but with aberrant structure. The Δcj1461 mutant was sevenfold more adherent to but 50-fold less invasive of INT-407 human epithelial cells than the wild type.

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 Role of DNA methylation in expression control of the IKZF3-GSDMA region in human epithelial cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0172707 ◽  
Author(s):  
Sanny Moussette ◽  
Abeer Al Tuwaijri ◽  
Hamid-Reza Kohan-Ghadr ◽  
Samar Elzein ◽  
Raquel Farias ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Epithelial Cells ◽  
Expression Control ◽  
Human Epithelial Cells

scholarly journals Stimulation of mucin exocytosis from human epithelial cells by nitric oxide: evidence for a cGMP-dependent and a cGMP-independent pathway

1997 ◽  
Vol 323 (2) ◽  
pp. 521-524 ◽  
Author(s):  
Jean-Eric BRANKA ◽  
Geneviève VALLETTE ◽  
Anne JARRY ◽  
Christian L. LABOISSE
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Soluble Guanylate Cyclase ◽  
Specific Inhibitor ◽  
Intracellular Signalling Pathway ◽  
Intracellular Cgmp ◽  
Human Epithelial Cells ◽  
Cellular Target ◽  
Combined Action

The aim of this work was to investigate the role of nitric oxide (NO) on the macromolecular exocytotic function of human epithelial cells. We tested the effects of two NO-generating drugs, i.e. 1-hexanamine 6-(2-hydroxy-1-methyl-2-nitrosohydrazine)-N-methyl (MAHMA NONOate) and sodium nitroprusside (SNP), on mucin exocytosis from the human colonic epithelial HT29-Cl.16E cell line. Our results show that MAHMA NONOate and SNP elicited a rapid mucin exocytotic response through a cGMP-dependent and a cGMP-independent pathway respectively. Indeed, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ), a newly available specific inhibitor of soluble guanylate cyclase, inhibited both cGMP accumulation and subsequent mucin exocytosis evoked by MAHMA NONOate. By contrast, SNP did not alter intracellular cGMP levels, and SNP-mediated mucin exocytosis was not inhibited by ODQ. As expected from two NO donors acting through distinct pathways, the combined action of MAHMA NONOate and SNP led to an additive effect on mucin exocytosis. SNP was likely to act through S-nitrosylation of a cellular target, because cysteine, a reductive thiol that provides decoy targets for SNP through the formation of nitrosocysteine, abolished the early stimulatory effect of SNP on mucin exocytosis. Finally, the fact that in the presence of cysteine SNP was able to trigger a late, ODQ-inhibitable, mucin exocytotic response demonstrates the ability of NO to shift its intracellular signalling pathway depending on the changes of the redox state of the milieu.

scholarly journals Identification of Campylobacter jejuni Genes Involved in Its Interaction with Epithelial Cells

2010 ◽  
Vol 78 (8) ◽  
pp. 3540-3553 ◽  
Author(s):  
Veronica Novik ◽  
Dirk Hofreuter ◽  
Jorge E. Galán
Keyword(s):  
Animal Model ◽  
Epithelial Cells ◽  
Host Cell ◽  
Campylobacter Jejuni ◽  
Host Cells ◽  
Drastic Reduction ◽  
Mutagenesis Screen ◽  
Infectious Gastroenteritis ◽  
Industrialized Nations ◽  
Host Cell Interactions

ABSTRACT Campylobacter jejuni is the leading cause of infectious gastroenteritis in industrialized nations. Its ability to enter and survive within nonphagocytic cells is thought to be very important for pathogenesis. However, little is known about the C. jejuni determinants that mediate these processes. Through an extensive transposon mutagenesis screen, we have identified several loci that are required for C. jejuni efficient entry and survival within epithelial cells. Among these loci, insertional mutations in aspA, aspB, and sodB resulted in drastic reduction in C. jejuni entry and/or survival within host cells and a severe defect in colonization in an animal model. The implications of these findings for the understanding of C. jejuni-host cell interactions are discussed.

scholarly journals Role of flm Locus in MesophilicAeromonas Species Adherence

2001 ◽  
Vol 69 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Ioannis Gryllos ◽  
Jonathan G. Shaw ◽  
Rosalina Gavı́n ◽  
Susana Merino ◽  
Juan M. Tomás
Keyword(s):  
Epithelial Cells ◽  
Aeromonas Caviae ◽  
Human Epithelial Cells ◽  
Putative Operon ◽  
Adherence Mechanism ◽  
Transposon Insertions ◽  
Flagella Assembly ◽  
Insertion Mutants

ABSTRACT The adherence mechanism of Aeromonas caviae Sch3N to HEp-2 cells was initially investigated through four mini-Tn5 mutants that showed a 10-fold decrease in adherence. These mutants lost motility, flagella, and their lipopolysaccharide (LPS) O antigen (O-Ag). Three genes,flmB-neuA-flmD, were found to be interrupted by the transposon insertions; additionally, two other genes, one lying upstream (flmA) and one downstream (neuB), were found to be clustered in the same operon. While the flmAand flmB genes were present in all mesophilicAeromonas spp. (A. hydrophila, A. caviae, A. veronii bv. veronii, andA. veronii bv. sobria) tested, this was not the case for the neuA-flmD-neuB genes. Construction and characterization of flmB insertion mutants in five other mesophilic Aeromonas strains revealed the loss of motility, flagella, and adherence but did not alter the LPS composition of these strains. Taking the above findings into consideration, we conclude (i) that flagella and possibly the LPS O-Ag are involved in the adherence of the mesophilic Aeromonas to human epithelial cells; (ii)flmA and flmB are genes widely distributed in the mesophilic Aeromonas and are involved in flagella assembly, and thus adherence; and (iii) in A. caviae Sch3N the flmA and flmB genes are found in a putative operon together with neuA, flmD, andneuB and are involved in LPS O-Ag biosynthesis and probably have a role in flagellum assembly.

scholarly journals Role of the Gonococcal Neisserial Heparin Binding Antigen in Microcolony Formation, and Serum Resistance and Adherence to Epithelial Cells

2019 ◽  
Vol 221 (10) ◽  
pp. 1612-1622 ◽  
Author(s):  
Evgeny A Semchenko ◽  
Tsitsi D Mubaiwa ◽  
Christopher J Day ◽  
Kate L Seib
Keyword(s):  
Epithelial Cells ◽  
Cell Aggregation ◽  
Host Cells ◽  
Heparin Binding ◽  
Transmitted Infection ◽  
Sexually Transmitted ◽  
Treatment And Prevention ◽  
New Treatment ◽  
Reduced Adherence

Abstract The sexually transmitted infection gonorrhoea is on the rise worldwide and an increased understanding of the mechanisms of colonization and pathogenesis of Neisseria gonorrhoeae is required to aid development of new treatment and prevention strategies. In the current study, we investigate the neisserial heparin-binding antigen (NHBA) of N. gonorrhoeae and confirm its role in binding to several glycans, including heparin, and identify interactions of NHBA with both gonococcal and host cells. Furthermore, we report that a gonococcal nhba mutant displays decreased cell aggregation and microcolony formation, as well as reduced survival in human serum and reduced adherence to human cervical and urethral epithelial cells, relative to the wild-type strain. These data indicate that the gonococcal NHBA contributes to several aspects of the colonization and survival of N. gonorrhoeae and may be a target for new antimicrobial or vaccines.

Balance of bacterial pro- and anti-inflammatory mediators dictates net effect of enteropathogenicEscherichia colion intestinal epithelial cells

2006 ◽  
Vol 290 (4) ◽  
pp. G685-G694 ◽  
Author(s):  
Rachna Sharma ◽  
Samuel Tesfay ◽  
Farol L. Tomson ◽  
Rajani P. Kanteti ◽  
V. K. Viswanathan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Host Cells ◽  
Intestinal Epithelial ◽  
E Coli ◽  
Inflammatory Proteins ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Prior Infection

Enteropathogenic Escherichia coli (EPEC) virulence requires a type III secretion system (TTSS) to deliver effector molecules in host cells. Although the TTSS is crucial to EPEC pathogenesis, its function in EPEC-induced inflammation is not known. The aim of this study was to investigate the role of the TTSS in EPEC-induced inflammation. HT-29 intestinal epithelial cells were infected with wild-type (WT) EPEC or select mutant strains or exposed to corresponding filter-sterilized supernatants (SN), and interleukin-8 (IL-8) secretion was determined by ELISA. EPEC SN stimulated significantly greater IL-8 production than EPEC organisms. Flagellin, as well as a TTSS-independent >50-kDa nonflagellin protein, was found to significantly contribute to this response. Dose-response studies showed that increasing concentrations of WT SN proportionally increased IL-8, whereas increasing multiplicity of infection of EPEC inversely correlated with IL-8 secretion, suggesting that EPEC dampens this host response. Infection with Δ escN (nonfunctional TTSS) markedly increased IL-8 compared with WT, indicating that a functional TTSS is required for this anti-inflammatory property; complementation of escN restored the attenuated response. Mutation of espB also enhanced the IL-8 response, and complementation returned IL-8 to near WT levels, suggesting involvement of this effector. The anti-inflammatory effect extends to both bacterial and host-derived proinflammatory stimuli, since prior infection with EPEC suppressed the IL-8 response to tumor necrosis factor-α, IL-1β, and enterohemorrhagic E. coli flagellin. These findings indicate that EPEC-induced inflammation is a balance between pro- and anti-inflammatory proteins; extracellular factors, including flagellin and an unidentified TTSS-independent, >50-kDa protein, trigger inflammation while intracellular TTSS-dependent factors, including EspB, attenuate this response.

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