scholarly journals Role of Protein Glycosylation in Host-Pathogen Interaction

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1022 ◽  
Author(s):  
Borong Lin ◽  
Xue Qing ◽  
Jinling Liao ◽  
Kan Zhuo

Host-pathogen interactions are fundamental to our understanding of infectious diseases. Protein glycosylation is one kind of common post-translational modification, forming glycoproteins and modulating numerous important biological processes. It also occurs in host-pathogen interaction, affecting host resistance or pathogen virulence often because glycans regulate protein conformation, activity, and stability, etc. This review summarizes various roles of different glycoproteins during the interaction, which include: host glycoproteins prevent pathogens as barriers; pathogen glycoproteins promote pathogens to attack host proteins as weapons; pathogens glycosylate proteins of the host to enhance virulence; and hosts sense pathogen glycoproteins to induce resistance. In addition, this review also intends to summarize the roles of lectin (a class of protein entangled with glycoprotein) in host-pathogen interactions, including bacterial adhesins, viral lectins or host lectins. Although these studies show the importance of protein glycosylation in host-pathogen interaction, much remains to be discovered about the interaction mechanism.

2010 ◽  
Vol 63 (4) ◽  
pp. 322-329 ◽  
Author(s):  
Celso A Reis ◽  
Hugo Osorio ◽  
Luisa Silva ◽  
Catarina Gomes ◽  
Leonor David

Glycoconjugates constitute a major class of biomolecules which include glycoproteins, glycosphingolipids and proteoglycans. Glycans are involved in several physiological and pathological conditions, such as host–pathogen interactions, cell differentiation, migration, tumour invasion and metastisation, cell trafficking and signalling. Cancer is associated with glycosylation alterations in glycoproteins and glycolipids. This review describes various aspects of protein glycosylation with the focus on alterations associated with human cancer. The application of these glycosylation modifications as biomarkers for cancer detection in tumour tissues and serological assays is summarised.


1999 ◽  
Vol 22 (4) ◽  
pp. 601-608
Author(s):  
Leonardo Cunha Melo ◽  
João Bosco dos Santos

Plant resistance to pathogens is the most efficient form of disease control. However, identification of resistant genotypes is often difficult, especially when the genetic basis for the host-pathogen relationship is unknown. This study was carried out to test a methodology capable of providing, in a simple way, information about host vertical and horizontal resistance as well as pathogen virulence. A simulation using twenty, ten, and five pathogen races and twenty hosts was carried out. Host reaction was controlled by ten genes with two alleles each. Eight genes had little effects, one had medium and the other strong effects. Genetic control of pathogenicity was identical to that of the host. Only homozygous genotypes were used for pathogens and hosts in this simulation, with no epistatic effects. Simulation was based on the expected disease severity with the inoculation of twenty hosts with twenty pathogen races, according to additive and interactive models proposed by Parlevliet and Zadoks (Euphytica 26: 5-21, 1977). Data were analyzed by model IV of Griffing, using a partial diallel scheme. A high correlation was found between general reaction ability (GRA) and potential host resistance, which proved to be an indicator of horizontal resistance. A high correlation between general aggressivity ability (GAA) and potential pathogenicity of the race also proved to be an aggressivity indicator. Specific interaction ability (SIA) is an indicator of host vertical resistance and pathogen virulence. Simulation with a lower number of races (ten and five) showed similar results. SIA was significant in both the interactive and additive models.


2013 ◽  
Vol 11 (02) ◽  
pp. 1230001 ◽  
Author(s):  
HUFENG ZHOU ◽  
JINGJING JIN ◽  
LIMSOON WONG

Host–pathogen interactions are important for understanding infection mechanism and developing better treatment and prevention of infectious diseases. Many computational studies on host–pathogen interactions have been published. Here, we review recent progress and results in this field and provide a systematic summary, comparison and discussion of computational studies on host–pathogen interactions, including prediction and analysis of host–pathogen protein–protein interactions; basic principles revealed from host–pathogen interactions; and database and software tools for host–pathogen interaction data collection, integration and analysis.


Author(s):  
Bob J. Ignacio ◽  
Thomas Bakkum ◽  
Kimberly M. Bonger ◽  
Nathaniel I. Martin ◽  
Sander I. van Kasteren

Metabolic labeling of intracellular pathogens can provide new methods of studying host pathogen interactions.


2019 ◽  
Author(s):  
Cristina Y. Zamora ◽  
Elizabeth M. Ward ◽  
Jemila C. Kester ◽  
Wen Li Kelly Chen ◽  
Jason G. Velazquez ◽  
...  

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.


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 ◽  
...  

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.


Author(s):  
D. NIHARIKA ◽  
B. NIHARIKA ◽  
T. AISHWARYA ◽  
A. NIKITHA ◽  
RABIA BUTOOL ◽  
...  

Viruses can infect almost all the types of life forms, from animals, plants to microorganisms. They are found in almost every ecosystem on Earth and are the most numerous types of biological entity. The present pandemic on Earth due to SARS COV 2, coronavirus has given a big jolt to the scientific community and created a deep curiosity in us to understand the virus and its interaction biochemically in humans. We did a small project by researching and compiling the information about its outbreak and host-pathogen interactions. To understand this pandemic COVID 19 and the virus, we as students learnt the structural morphology of virus and its role in the host-pathogen interaction. We used several online platforms for our study like PubMed, Scopus, WHO, ICMR and CDC Websites.


2019 ◽  
Vol 32 (3) ◽  
Author(s):  
Jennifer A. Grousd ◽  
Helen E. Rich ◽  
John F. Alcorn

SUMMARY Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. Despite broad literature including basic and translational scientific studies, many gaps in our understanding of host-pathogen interactions remain. In this review, pathogen virulence factors that drive lung infection and injury are discussed in relation to their associated host immune pathways. CAP epidemiology is considered, with a focus on Staphylococcus aureus and Streptococcus pneumoniae as primary pathogens. Bacterial factors involved in nasal colonization and subsequent virulence are illuminated. A particular emphasis is placed on bacterial pore-forming toxins, host cell death, and inflammasome activation. Identified host-pathogen interactions are then examined by linking pathogen factors to aberrant host response pathways in the context of acute lung injury in both primary and secondary infection. While much is known regarding bacterial virulence and host immune responses, CAP management is still limited to mostly supportive care. It is likely that improvements in therapy will be derived from combinatorial targeting of both pathogen virulence factors and host immunomodulation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Khushboo Borah ◽  
Ye Xu ◽  
Johnjoe McFadden

Tuberculosis (TB) is a devastating infectious disease that kills over a million people every year. There is an increasing burden of multi drug resistance (MDR) and extensively drug resistance (XDR) TB. New and improved therapies are urgently needed to overcome the limitations of current treatment. The causative agent, Mycobacterium tuberculosis (Mtb) is one of the most successful pathogens that can manipulate host cell environment for adaptation, evading immune defences, virulence, and pathogenesis of TB infection. Host-pathogen interaction is important to establish infection and it involves a complex set of processes. Metabolic cross talk between the host and pathogen is a facet of TB infection and has been an important topic of research where there is growing interest in developing therapies and drugs that target these interactions and metabolism of the pathogen in the host. Mtb scavenges multiple nutrient sources from the host and has adapted its metabolism to survive in the intracellular niche. Advancements in systems-based omic technologies have been successful to unravel host-pathogen interactions in TB. In this review we discuss the application and usefulness of omics in TB research that provides promising interventions for developing anti-TB therapies.


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