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Recognition, survival and persistence of Staphylococcus aureus in the model host Tenebrio molitor

X0145305X

X0145305X

Jack Dorling and Caroline Moraes and Jens Rolff – 2015

The degree of specificity of any given immune response to a parasite is governed by the complexity and variation of interactions between host and pathogen derived molecules. Here, we assess the extent to which recognition and immuno-resistance of cell wall mutants of the pathogen Staphylococcus aureus may contribute to establishment and maintenance of persistent infection in the model insect host, Tenebrio molitor. The cell surface of S. aureus is decorated with various molecules, including glycopolymers such as wall teichoic acid (WTA). WTA is covalently bound to peptidoglycan (PGN) and its absence has been associated with increased recognition of PGN by host receptors (PGRPs). WTA is also further modified by other molecules such as D-alanine (D-alanylation). Both the level of WTA expression and its D-alanylation were found to be important in the mediation of the host–parasite interaction in this model system. Specifically, WTA itself was seen to influence immune recognition, while D-alanylation of WTA was found to increase immuno-resistance and was associated with prolonged persistence of S. aureus in T. molitor. These results implicate WTA and its D-alanylation as important factors in the establishment and maintenance of persistent infection, affecting different critical junctions in the immune response; through potential evasion of recognition by PGRPs and resistance to humoral immune effectors during prolonged exposure to the immune system. This highlights a mechanism by which specificity in this host–parasite interaction may arise.

Titel
Recognition, survival and persistence of Staphylococcus aureus in the model host Tenebrio molitor
Verfasser
Jack Dorling and Caroline Moraes and Jens Rolff
Verlag
Developmental & Comparative Immunology
Datum
2015
Kennung
https://doi.org/10.1016/j.dci.2014.08.010
Sprache
eng
Art
Text
BibTeX Code
@article{DORLING2015284,
title = {Recognition, survival and persistence of Staphylococcus aureus in the model host Tenebrio molitor},
journal = {Developmental & Comparative Immunology},
volume = {48},
number = {2},
pages = {284-290},
year = {2015},
note = {Specific immunity in invertebrates},
issn = {0145-305X},
doi = {https://doi.org/10.1016/j.dci.2014.08.010},
url = {https://www.sciencedirect.com/science/article/pii/S0145305X14002237},
author = {Jack Dorling and Caroline Moraes and Jens Rolff},
keywords = {Persistence, Wall teichoic acids, Antimicrobial peptides},
abstract = {The degree of specificity of any given immune response to a parasite is governed by the complexity and variation of interactions between host and pathogen derived molecules. Here, we assess the extent to which recognition and immuno-resistance of cell wall mutants of the pathogen Staphylococcus aureus may contribute to establishment and maintenance of persistent infection in the model insect host, Tenebrio molitor. The cell surface of S. aureus is decorated with various molecules, including glycopolymers such as wall teichoic acid (WTA). WTA is covalently bound to peptidoglycan (PGN) and its absence has been associated with increased recognition of PGN by host receptors (PGRPs). WTA is also further modified by other molecules such as D-alanine (D-alanylation). Both the level of WTA expression and its D-alanylation were found to be important in the mediation of the host–parasite interaction in this model system. Specifically, WTA itself was seen to influence immune recognition, while D-alanylation of WTA was found to increase immuno-resistance and was associated with prolonged persistence of S. aureus in T. molitor. These results implicate WTA and its D-alanylation as important factors in the establishment and maintenance of persistent infection, affecting different critical junctions in the immune response; through potential evasion of recognition by PGRPs and resistance to humoral immune effectors during prolonged exposure to the immune system. This highlights a mechanism by which specificity in this host–parasite interaction may arise.}
}