scholarly journals Genetic background of IL-10−/− mice alters host–pathogen interactions with Campylobacter jejuni and influences disease phenotype

2008 ◽  
Vol 45 (4) ◽  
pp. 241-257 ◽  
Author(s):  
L.S. Mansfield ◽  
J.S. Patterson ◽  
B.R. Fierro ◽  
A.J. Murphy ◽  
V.A. Rathinam ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Genetic Background ◽  
Disease Phenotype ◽  
Host Pathogen Interactions ◽  
Host Pathogen

scholarly journals Application of a gut-immune co-culture system for the study of N-glycan-dependent host-pathogen interactions of Campylobacter jejuni

2019 ◽  
Author(s):  
Cristina Y. Zamora ◽  
Elizabeth M. Ward ◽  
Jemila C. Kester ◽  
Wen Li Kelly Chen ◽  
Jason G. Velazquez ◽  
...  
Keyword(s):  
Immune System ◽  
Campylobacter Jejuni ◽  
Outer Membrane Vesicles ◽  
Protein Glycosylation ◽  
Bacterial Invasion ◽  
Host Pathogen Interactions ◽  
Barrier Functions ◽  
Immune System Activation ◽  
Culture Model ◽  
Host Pathogen

AbstractAn in vitro gut-immune co-culture model with apical and basal accessibility, designed to more closely resemble a human intestinal microenvironment, was employed to study the role of the Nlinked protein glycosylation (Pgl) pathway in Campylobacter jejuni pathogenicity. The gutimmune co-culture (GIC) was developed to model important aspects of the human small intestine by the inclusion of mucin producing goblet cells, human enterocytes, and dendritic cells, bringing together a mucus-containing epithelial monolayer with elements of the innate immune system. The utility of the system was demonstrated by characterizing host-pathogen interactions facilitated by N-linked glycosylation, such as host epithelial barrier functions, bacterial invasion and immunogenicity. Changes in human intestinal barrier functions in the presence of 11168 C. jejuni (wildtype) strains were quantified using GICs. The glycosylationdeficient strain 11168 ΔpglE was 100-fold less capable of adhering to and invading this intestinal model in cell infectivity assays. Quantification of inflammatory signaling revealed that 11168ΔpglE differentially modulated inflammatory responses in different intestinal microenvironments, suppressive in some but activating in others. Virulence-associated outer membrane vesicles produced by wildtype and 11168ΔpglE C. jejuni were shown to have differential composition and function, with both leading to immune system activation when provided to the gut-immune co-culture model. This analysis of aspects of C. jejuni infectivity in the presence and absence of its N-linked glycome, is enabled by application of the gut-immune model and we anticipate that this system will be applicable to further studies of C. jejuni and other enteropathogens of interest.

scholarly journals Application of a gut-immune co-culture system for the study of N-glycan-dependent host–pathogen interactions of Campylobacter jejuni

Glycobiology ◽  
2020 ◽  
Vol 30 (6) ◽  
pp. 374-381 ◽  
Author(s):  
Cristina Y Zamora ◽  
Elizabeth M Ward ◽  
Jemila C Kester ◽  
Wen Li Kelly Chen ◽  
Jason G Velazquez ◽  
...  
Keyword(s):  
Immune System ◽  
Campylobacter Jejuni ◽  
Outer Membrane Vesicles ◽  
Protein Glycosylation ◽  
Bacterial Invasion ◽  
Host Pathogen Interactions ◽  
Barrier Functions ◽  
Immune System Activation ◽  
Culture Model ◽  
Host Pathogen

Abstract An in vitro gut-immune co-culture model with apical and basal accessibility, designed to more closely resemble a human intestinal microenvironment, was employed to study the role of the N-linked protein glycosylation pathway in Campylobacter jejuni pathogenicity. The gut-immune co-culture (GIC) was developed to model important aspects of the human small intestine by the inclusion of mucin-producing goblet cells, human enterocytes and dendritic cells, bringing together a mucus-containing epithelial monolayer with elements of the innate immune system. The utility of the system was demonstrated by characterizing host–pathogen interactions facilitated by N-linked glycosylation, such as host epithelial barrier functions, bacterial invasion and immunogenicity. Changes in human intestinal barrier functions in the presence of 11168 C. jejuni (wildtype) strains were quantified using GICs. The glycosylation-impaired strain 11168 ΔpglE was 100-fold less capable of adhering to and invading this intestinal model in cell infectivity assays. Quantification of inflammatory signaling revealed that 11168ΔpglE differentially modulated inflammatory responses in different intestinal microenvironments, suppressive in some but activating in others. Virulence-associated outer membrane vesicles produced by wildtype and 11168ΔpglE C. jejuni were shown to have differential composition and function, with both leading to immune system activation when provided to the gut-immune co-culture model. This analysis of aspects of C. jejuni infectivity in the presence and absence of its N-linked glycome is enabled by application of the gut-immune model, and we anticipate that this system will be applicable to further studies of C. jejuni and other enteropathogens of interest.

Human Colonoids as a Model for Studying Host‐Pathogen Interactions with Campylobacter jejuni

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Adam L. Edwinson ◽  
Stephanie A. Peters ◽  
Margaret K. Breen-Lyles ◽  
Gianrico Farrugia ◽  
Madhusudan Grover
Keyword(s):  
Campylobacter Jejuni ◽  
Host Pathogen Interactions ◽  
Host Pathogen

Spatiotemporal Structure of Host-Pathogen Interactions in a Metapopulation

2009 ◽  
Vol 174 (3) ◽  
pp. 308
Author(s):  
Soubeyrand ◽  
Laine ◽  
Hanski ◽  
Penttinen
Keyword(s):  
Host Pathogen Interactions ◽  
Spatiotemporal Structure ◽  
Host Pathogen

scholarly journals Porcine small intestinal organoids as a model to explore ETEC–host interactions in the gut

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Bjarne Vermeire ◽  
Liara M. Gonzalez ◽  
Robert J. J. Jansens ◽  
Eric Cox ◽  
Bert Devriendt
Keyword(s):  
Intestinal Epithelial ◽  
Gut Health ◽  
Functional Responses ◽  
Host Pathogen Interactions ◽  
Epithelial Surface ◽  
Host Interactions ◽  
Intestinal Organoids ◽  
Host Pathogen ◽  
Small Intestinal

AbstractSmall intestinal organoids, or enteroids, represent a valuable model to study host–pathogen interactions at the intestinal epithelial surface. Much research has been done on murine and human enteroids, however only a handful studies evaluated the development of enteroids in other species. Porcine enteroid cultures have been described, but little is known about their functional responses to specific pathogens or their associated virulence factors. Here, we report that porcine enteroids respond in a similar manner as in vivo gut tissues to enterotoxins derived from enterotoxigenic Escherichia coli, an enteric pathogen causing postweaning diarrhoea in piglets. Upon enterotoxin stimulation, these enteroids not only display a dysregulated electrolyte and water balance as shown by their swelling, but also secrete inflammation markers. Porcine enteroids grown as a 2D-monolayer supported the adhesion of an F4+ ETEC strain. Hence, these enteroids closely mimic in vivo intestinal epithelial responses to gut pathogens and are a promising model to study host–pathogen interactions in the pig gut. Insights obtained with this model might accelerate the design of veterinary therapeutics aimed at improving gut health.

scholarly journals Movement can mediate temporal mismatches between resource availability and biological events in host–pathogen interactions

2021 ◽  
Author(s):  
Tobias Kürschner ◽  
Cédric Scherer ◽  
Viktoriia Radchuk ◽  
Niels Blaum ◽  
Stephanie Kramer‐Schadt
Keyword(s):  
Resource Availability ◽  
Host Pathogen Interactions ◽  
Host Pathogen

Convergent evolution and mimicry of protein linear motifs in host–pathogen interactions

2015 ◽  
Vol 32 ◽  
pp. 91-101 ◽  
Author(s):  
Lucía Beatriz Chemes ◽  
Gonzalo de Prat-Gay ◽  
Ignacio Enrique Sánchez
Keyword(s):  
Convergent Evolution ◽  
Host Pathogen Interactions ◽  
Host Pathogen ◽  
Linear Motifs
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