FB2026_02 , released June 18, 2026
FB2026_02 , released June 18, 2026
Reference Report
Open Close
Reference
Citation
Najjar, H., Al-Ashmar, S., Qush, A., Al-Asmar, J., Rashwan, S., Elgamal, A., Zeidan, A., Kamareddine, L. (2022). Enteric pathogens modulate metabolic homeostasis in the Drosophila melanogaster host.  Microbes Infect. 24(4): 104946.
FlyBase ID
FBrf0253531
Publication Type
Research paper
Abstract
On quotidian basis, living beings work out an armistice with their microbial flora and a scuffle with invading pathogens to maintain a normal state of health. Although producing virulence factors and escaping the host's immune machinery are the paramount tools used by pathogens in their "arm race" against the host; here, we provide insight into another facet of pathogenic embitterment by presenting evidence of the ability of enteric pathogens to exhibit pathogenicity through modulating metabolic homeostasis in Drosophila melanogaster. We report that Escherichia coli and Shigella sonnei orally infected flies exhibit lipid droplet deprivation from the fat body, irregular accumulation of lipid droplets in the midgut, and significant elevation of systemic glucose and triglyceride levels. Our findings indicate that these detected metabolic alterations in infected flies could be attributed to differential regulation of peptide hormones known to be crucial for lipid metabolism and insulin signaling. Gaining a proper understanding of infection-induced alterations succours in curbing the pathogenesis of enteric diseases and sets the stage for promising therapeutic approaches to quarry infection-induced metabolic disorders.
PubMed ID
PubMed Central ID
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Microbes Infect.
    Title
    Microbes and Infection
    Publication Year
    1999-
    ISBN/ISSN
    1286-4579
    Data From Reference
    Genes (3)
    Human Disease Models (2)