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Book ; Online ; Thesis: Remodelling of the F-actin Cytoskeleton of polarized epithelial cells by the type 3 secretion system-1 effector proteins of Salmonella enterica sv. Typhimurium

2022

Author's details	presented by: Alfonso Felipe-López, Diplom Chemist-Bacteriologist-Parasitologist, Esuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional Mexico
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Leipzig ; Deutsche Nationalbibliothek
Publishing place	Frankfurt am Main
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Manipulation of microvillar proteins during

Felipe-López, Alfonso / Hansmeier, Nicole / Danzer, Claudia / Hensel, Michael

Frontiers in cellular and infection microbiology

2023 Volume 13, Page(s) 1137062

Abstract: Enterocyte invasion by the gastrointestinal ... ...

Abstract	Enterocyte invasion by the gastrointestinal pathogen
MeSH term(s)	Actins/metabolism ; Salmonella enterica/metabolism ; Microvilli ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Actin Cytoskeleton/metabolism ; Salmonella/metabolism
Chemical Substances	Actins ; Bacterial Proteins
Language	English
Publishing date	2023-03-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2023.1137062
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cell death induction facilitates egress of Coxiella burnetii from infected host cells at late stages of infection.

Schulze-Luehrmann, Jan / Liebler-Tenorio, Elisabeth / Felipe-López, Alfonso / Lührmann, Anja

Molecular microbiology

2023 Volume 121, Issue 3, Page(s) 513–528

Abstract: Intracellular bacteria have evolved mechanisms to invade host cells, establish an intracellular niche that allows survival and replication, produce progeny, and exit the host cell after completion of the replication cycle to infect new target cells. ... ...

Abstract	Intracellular bacteria have evolved mechanisms to invade host cells, establish an intracellular niche that allows survival and replication, produce progeny, and exit the host cell after completion of the replication cycle to infect new target cells. Bacteria exit their host cell by (i) initiation of apoptosis, (ii) lytic cell death, and (iii) exocytosis. While bacterial egress is essential for bacterial spreading and, thus, pathogenesis, we currently lack information about egress mechanisms for the obligate intracellular pathogen C. burnetii, the causative agent of the zoonosis Q fever. Here, we demonstrate that C. burnetii inhibits host cell apoptosis early during infection, but induces and/or increases apoptosis at later stages of infection. Only at later stages of infection did we observe C. burnetii egress, which depends on previously established large bacteria-filled vacuoles and a functional intrinsic apoptotic cascade. The released bacteria are not enclosed by a host cell membrane and can infect and replicate in new target cells. In summary, our data argue that C. burnetii egress in a non-synchronous way at late stages of infection. Apoptosis-induction is important for C. burnetii egress, but other pathways most likely contribute.
MeSH term(s)	Humans ; Coxiella burnetii/metabolism ; Q Fever/metabolism ; Q Fever/microbiology ; Q Fever/pathology ; Apoptosis/physiology ; Signal Transduction ; Vacuoles/metabolism ; Host-Pathogen Interactions
Language	English
Publishing date	2023-12-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/mmi.15210
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Article ; Online: Cell death induction facilitates egress of Coxiella burnetii from infected host cells at late stages of infection

Schulze‐Luehrmann, Jan / Liebler‐Tenorio, Elisabeth / Felipe‐López, Alfonso / Lührmann, Anja

2023

Abstract	Intracellular bacteria have evolved mechanisms to invade host cells, establish an intracellular niche that allows survival and replication, produce progeny, and exit the host cell after completion of the replication cycle to infect new target cells. Bacteria exit their host cell by (i) initiation of apoptosis, (ii) lytic cell death, and (iii) exocytosis. While bacterial egress is essential for bacterial spreading and, thus, pathogenesis, we currently lack information about egress mechanisms for the obligate intracellular pathogen C. burnetii, the causative agent of the zoonosis Q fever. Here, we demonstrate that C. burnetii inhibits host cell apoptosis early during infection, but induces and/or increases apoptosis at later stages of infection. Only at later stages of infection did we observe C. burnetii egress, which depends on previously established large bacteria-filled vacuoles and a functional intrinsic apoptotic cascade. The released bacteria are not enclosed by a host cell membrane and can infect and replicate in new target cells. In summary, our data argue that C. burnetii egress in a non-synchronous way at late stages of infection. Apoptosis-induction is important for C. burnetii egress, but other pathways most likely contribute.
Keywords	article ; Text ; ddc:570 ; Coxiella burnetii -- Q fever -- apoptosis -- egress -- spreading
Subject code	570
Language	English
Publishing date	2023-12-19
Publisher	Wiley
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Book ; Thesis: Remodelling of the F-actin cytoskeleton of polarized epithelial cells by the type 3 secretion system-1 effector proteins of Salmonella enterica sv. Typhimurium

Felipe-López, Alfonso

2014

Author's details	presented by: Alfonso Felipe-López
Language	English
Size	11 Bl., S. 12 - 229, Bl. 230 - 237, Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Osnabrück, 2014
Note	Kumulative Dissertation, enthält 4 Beiträge
Accompanying material	1 CD-ROM (12 cm)
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article: A Plasmid-Encoded FetMP-Fls Iron Uptake System Confers Selective Advantages to

García, Vanesa / Herrero-Fresno, Ana / Rodicio, Rosaura / Felipe-López, Alfonso / Montero, Ignacio / Olsen, John E / Hensel, Michael / Rodicio, María Rosario

Microorganisms

2020 Volume 8, Issue 5

Abstract: The resistance plasmid pUO-StVR2, derived from virulence plasmid pSLT, is widespread in clinical isolates ... ...

Abstract	The resistance plasmid pUO-StVR2, derived from virulence plasmid pSLT, is widespread in clinical isolates of
Language	English
Publishing date	2020-04-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8050630
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Article: A Plasmid-Encoded FetMP-Fls Iron Uptake System Confers Selective Advantages to Salmonella enterica Serovar Typhimurium in Growth under Iron-Restricted Conditions and for Infection of Mammalian Host Cells

García, Vanesa / Herrero-Fresno, Ana / Rodicio, Rosaura / Felipe-López, Alfonso / Montero, Ignacio / Olsen, John E. / Hensel, Michael / Rodicio, María Rosario

Microorganisms. 2020 Apr. 27, v. 8, no. 5

2020

Abstract: The resistance plasmid pUO-StVR2, derived from virulence plasmid pSLT, is widespread in clinical isolates of Salmonella enterica serovar Typhimurium recovered in Spain and other European countries. pUO-StVR2 carries several genes encoding a FetMP-Fls ... ...

Abstract	The resistance plasmid pUO-StVR2, derived from virulence plasmid pSLT, is widespread in clinical isolates of Salmonella enterica serovar Typhimurium recovered in Spain and other European countries. pUO-StVR2 carries several genes encoding a FetMP-Fls system, which could be involved in iron uptake. We therefore analyzed S. Typhimurium LSP 146/02, a clinical strain selected as representative of the isolates carrying the plasmid, and an otherwise isogenic mutant lacking four genes (fetMP-flsDA) of the fetMP-fls region. Growth curves and determination of the intracellular iron content under iron-restricted conditions demonstrated that deletion of these genes impairs iron acquisition. Thus, under these conditions, the mutant grew significantly worse than the wild-type strain, its iron content was significantly lower, and it was outcompeted by the wild-type strain in competition assays. Importantly, the strain lacking the fetMP-flsDA genes was less invasive in cultured epithelial HeLa cells and replicated poorly upon infection of RAW264.7 macrophages. The genes were introduced into S. Typhimurium ATCC 14028, which lacks the FetMP-Fls system, and this resulted in increased growth under iron limitation as well as an increased ability to multiply inside macrophages. These findings indicate that the FetMP-Fls iron acquisition system exceeds the benefits conferred by the other high-affinity iron uptake systems carried by ATCC 14028 and LSP 146/02. We proposed that effective iron acquisition by this system in conjunction with antimicrobial resistance encoded from the same plasmid have greatly contributed to the epidemic success of S. Typhimurium isolates harboring pUO-StVR2.
Keywords	Salmonella Typhimurium ; antibiotic resistance ; epithelium ; macrophages ; mammals ; mutants ; plasmids ; virulence ; Spain
Language	English
Dates of publication	2020-0427
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8050630
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Salmonella enterica invasion of polarized epithelial cells is a highly cooperative effort.

Lorkowski, Martin / Felipe-López, Alfonso / Danzer, Claudia A / Hansmeier, Nicole / Hensel, Michael

Infection and immunity

2014 Volume 82, Issue 6, Page(s) 2657–2667

Abstract: The invasion of polarized epithelial cells by Salmonella enterica requires the cooperative activity of the Salmonella pathogenicity island 1 (SPI1)-encoded type III secretion system (T3SS) and the SPI4-encoded adhesin SiiE. The invasion of polarized ... ...

Abstract	The invasion of polarized epithelial cells by Salmonella enterica requires the cooperative activity of the Salmonella pathogenicity island 1 (SPI1)-encoded type III secretion system (T3SS) and the SPI4-encoded adhesin SiiE. The invasion of polarized cells is more efficient than that of nonpolarized cells, and we observed the formation of clusters of bacteria on infected cells. Here we demonstrate that the invasion of polarized cells is a highly cooperative activity. Using a novel live-cell imaging approach, we visualized the cooperative entry of multiple bacteria into ruffles induced on the apical surfaces of polarized cells. The induction of membrane ruffles by activity of Salmonella enables otherwise noninvasive mutant strains to enter polarized host cells. Bacterial motility and chemotaxis were of lower importance for cooperativity in polarized-cell invasion. We propose that cooperative invasion is a key factor for the very efficient entry into polarized cells and a factor contributing to epithelial damage and intestinal inflammation.
MeSH term(s)	Cell Line ; Cell Movement/physiology ; Cell Polarity/physiology ; Chemotaxis/physiology ; Epithelial Cells/microbiology ; Epithelial Cells/physiology ; Host-Pathogen Interactions/physiology ; Humans ; Kidney/cytology ; Microscopy, Atomic Force ; Salmonella enterica/pathogenicity ; Salmonella enterica/physiology
Language	English
Publishing date	2014-04-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00023-14
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Zs.A 684: Show issues

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Article ; Online: Homoectoine Protects Against Colitis by Preventing a Claudin Switch in Epithelial Tight Junctions.

Castro-Ochoa, Karla F / Vargas-Robles, Hilda / Chánez-Paredes, Sandra / Felipe-López, Alfonso / Cabrera-Silva, Rodolfo I / Shibayama, Mineko / Betanzos, Abigail / Nava, Porfirio / Galinski, Erwin A / Schnoor, Michael

Digestive diseases and sciences

2018 Volume 64, Issue 2, Page(s) 409–420

Abstract: Background: Inflammatory bowel diseases (IBD) are multifactorial disorders affecting millions of people worldwide with alarmingly increasing incidences every year. Dysfunction of the intestinal epithelial barrier is associated with IBD pathogenesis, and ...

Abstract	Background: Inflammatory bowel diseases (IBD) are multifactorial disorders affecting millions of people worldwide with alarmingly increasing incidences every year. Dysfunction of the intestinal epithelial barrier is associated with IBD pathogenesis, and therapies include anti-inflammatory drugs that enhance intestinal barrier function. However, these drugs often have adverse side effects thus warranting the search for alternatives. Compatible solutes such as bacterial ectoines stabilize cell membranes and proteins. Aim: To unravel whether ectoine (1,4,5,6-tetrahydro-2-methyl-4-pyrimidinecarboxylic acid) and homoectoine (4,5,6,7-tetrahydro-2-methyl-1H-(1,3)-diazepine-4-carboxylic acid), a synthetic derivative of ectoine, have beneficial effects during dextran sulfate sodium (DSS)-induced colitis in mice. Methods/results: We found that the disease activity index was significantly reduced by both ectoines. DSS-induced edema formation, epithelial permeability, leukocyte recruitment and tissue damage were reduced by ectoine and homoectoine, with the latter having stronger effects. Interestingly, the claudin switch usually observed during colitis (decreased expression of claudin-1 and increased expression of the leaky claudin-2) was completely prevented by homoectoine, whereas ectoine only reduced claudin-2 expression. Concomitantly, only homoectoine ameliorated the drop in transepithelial electrical resistance induced by IFN-γ and TNF-α in Caco-2 cells. Both ectoines inhibited loss of ZO-1 and occludin and prevented IFN-γ/TNF-α-induced increased paracellular flux of 4 kDa FITC-dextran in vitro. Moreover, both ectoines reduced expression of pro-inflammatory cytokines and oxidative stress during colitis. Conclusion: While both ectoine and homoectoine have protective effects on the epithelial barrier during inflammation, only homoectoine completely prevented the inflammatory claudin switch in tight junctions. Thus, homoectoine may serve as diet supplement in IBD patients to reach or extend remission.
MeSH term(s)	Amino Acids, Diamino/pharmacology ; Animals ; Caco-2 Cells ; Claudin-1/drug effects ; Claudin-1/genetics ; Claudin-1/metabolism ; Claudin-2/drug effects ; Claudin-2/genetics ; Claudin-2/metabolism ; Colitis/chemically induced ; Colitis/metabolism ; Colitis/pathology ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Edema ; Electric Impedance ; Epithelium/drug effects ; Humans ; In Vitro Techniques ; Interferon-gamma/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Fluorescence ; Oxidative Stress/drug effects ; Permeability/drug effects ; Reverse Transcriptase Polymerase Chain Reaction ; Tight Junctions/drug effects ; Tight Junctions/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Amino Acids, Diamino ; Claudin-1 ; Claudin-2 ; Tumor Necrosis Factor-alpha ; homoectoine ; ectoine (7GXZ3858RY) ; Interferon-gamma (82115-62-6) ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2018-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-018-5309-8
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Article ; Online: High cortactin expression in B-cell acute lymphoblastic leukemia is associated with increased transendothelial migration and bone marrow relapse.

Velázquez-Avila, Martha / Balandrán, Juan Carlos / Ramírez-Ramírez, Dalia / Velázquez-Avila, Mirella / Sandoval, Antonio / Felipe-López, Alfonso / Nava, Porfirio / Alvarado-Moreno, José Antonio / Dozal, David / Prieto-Chávez, Jessica L / Schaks, Matthias / Rottner, Klemens / Dorantes-Acosta, Elisa / López-Martínez, Briceida / Schnoor, Michael / Pelayo, Rosana

Leukemia

2018 Volume 33, Issue 6, Page(s) 1337–1348

Abstract: Cancer is a major cause of death in children worldwide, with B-lineage cell acute lymphoblastic leukemia (B-ALL) being the most frequent childhood malignancy. Relapse, treatment failure and organ infiltration worsen the prognosis, warranting a better ... ...

Abstract	Cancer is a major cause of death in children worldwide, with B-lineage cell acute lymphoblastic leukemia (B-ALL) being the most frequent childhood malignancy. Relapse, treatment failure and organ infiltration worsen the prognosis, warranting a better understanding of the implicated mechanisms. Cortactin is an actin-binding protein involved in cell adhesion and migration that is overexpressed in many solid tumors and in adult B-cell chronic lymphocytic leukemia. Here, we investigated cortactin expression and potential impact on infiltration and disease prognosis in childhood B-ALL. B-ALL cell lines and precursor cells from bone marrow (BM) and cerebrospinal fluid (CSF) of B-ALL patients indeed overexpressed cortactin. In CXCL12-induced transendothelial migration assays, transmigrated B-ALL cells had highest cortactin expression. In xenotransplantation models, only cortactin
MeSH term(s)	Adolescent ; Animals ; Apoptosis ; Biomarkers, Tumor/metabolism ; Bone Marrow Neoplasms/metabolism ; Bone Marrow Neoplasms/pathology ; Cell Proliferation ; Child ; Child, Preschool ; Cortactin/metabolism ; Female ; Follow-Up Studies ; Gene Expression Regulation, Neoplastic ; Humans ; Infant ; Infant, Newborn ; Male ; Mice ; Mice, Nude ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Prognosis ; Survival Rate ; Transendothelial and Transepithelial Migration ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers, Tumor ; CTTN protein, human ; Cortactin
Language	English
Publishing date	2018-12-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-018-0333-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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