Metabolic homeostasis in chronic helminth infection is sustained by organ-specific metabolic rewiring

doi:10.1021/acsinfecdis.1c00026

Эндаумент фонд ТГУ!
Впиши своё имя в историю университета
- Сделать пожертвование -

Add to "Quick Collection"

Description	Size	Format
Metabolic homeostasis in chronic helminth infection is sustained by organ-specific metabolic rewiring	3 MB	Adobe Acrobat PDF	Read	Download
DOI Доступ к ресурсу на сайте издателя			10.1021/acsinfecdis.1c00026

#метаболомика

#ЯМР-спектроскопия

#описторхоз

#метаболическое ремоделирование

#хронические инфекции

Title: Metabolic homeostasis in chronic helminth infection is sustained by organ-specific metabolic rewiring
Creator: Kokova, Darya A.
|
Verhoeven, Aswin
|
Perina, Ekaterina A.
|
Ivanov, Vladimir V. (биолог)
|
Heijink, Marieke
|
Yazdanbakhsh, Maria
|
Mayboroda, Oleg A.
Date: 2021
DOI: 10.1021/acsinfecdis.1c00026
Description: Opisthorchiasis, is a hepatobiliary disease caused by flukes of the trematode family Opisthorchiidae. A chronic form of the disease implies a prolonged coexistence of a host and the parasite. The pathological changes inflicted by the worm to the host’s hepatobiliary system are well documented. Yet, the response to the infection also triggers a deep remodeling of the host systemic metabolism reaching a new homeostasis and affecting the organs beyond the worm location. Understanding the metabolic alternation in chronic opisthorchiasis, could help us to pinpoint pathways that underlie infection opening possibilities for the development of more selective treatment strategies. Here, with this report we apply an integrative, multicompartment metabolomics analysis, using multiple biofluids, stool samples and tissue extracts to describe metabolic changes in Opisthorchis felineus infected animals at the chronic stage. We show that the shift in lipid metabolism in the serum, a depletion of the amino acids pool, an alteration of the ketogenic pathways in the jejunum and a suppressed metabolic activity of the spleen are the key features of the metabolic host adaptation at the chronic stage of O. felineus infection. We describe this combination of the metabolic changes as a “metabolically mediated immunosuppressive status of organism” which develops during a chronic infection. This status in combination with other factors (e.g., parasite-derived immunomodulators) might increase risk of infection-related malignancy.