Extracellular adenosine modulates host-pathogen interactions through regulation of systemic metabolism during immune response in Drosophila

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F18%3A43897244" target="_blank" >RIV/60076658:12310/18:43897244 - isvavai.cz</a>

Result on the web

<a href="https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1007022&type=printable" target="_blank" >https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1007022&type=printable</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1371/journal.ppat.1007022" target="_blank" >10.1371/journal.ppat.1007022</a>

Result language

angličtina

Original language name

Extracellular adenosine modulates host-pathogen interactions through regulation of systemic metabolism during immune response in Drosophila

Original language description

Phagocytosis by hemocytes, Drosophila macrophages, is essential for resistance to Streptococcus pneumoniae in adult flies. Activated macrophages require an increased supply of energy and we show here that a systemic metabolic switch, involving the release of glucose from glycogen, is required for effective resistance to S. pneumoniae. This metabolic switch is mediated by extracellular adenosine, as evidenced by the fact that blocking adenosine signaling in the adoR mutant suppresses the systemic metabolic switch and decreases resistance to infection, while enhancing adenosine effects by lowering adenosine deaminase ADGF-A increases resistance to S. pneumoniae. Further, that ADGF-A is later expressed by immune cells during infection to regulate these effects of adenosine on the systemic metabolism and immune response. Such regulation proved to be important during chronic infection caused by Listeria monocytogenes. Lowering ADGF-A specifically in immune cells prolonged the systemic metabolic effects, leading to lower glycogen stores, and increased the intracellular load of L. monocytogenes, possibly by feeding the bacteria. An adenosine-mediated systemic metabolic switch is thus essential for effective resistance but must be regulated by ADGF-A expression from immune cells to prevent the loss of energy reserves and possibly to avoid the exploitation of energy by the pathogen.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10608 - Biochemistry and molecular biology

Project

<a href="/en/project/GA17-16406S" target="_blank" >GA17-16406S: Origin of adenosine as a selfish immunity signal</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

PLoS Pathogens

ISSN

1553-7366

e-ISSN

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Volume of the periodical

14

Issue of the periodical within the volume

4

Country of publishing house

US - UNITED STATES

Number of pages

26

Pages from-to

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UT code for WoS article

000431135400048

EID of the result in the Scopus database

2-s2.0-85046397700