Evaluating the Impact of Vitamin D 3 on NF-κB and JAK/STAT Signaling Pathways in Drosophila melanogaster .
Widya HardiyantiYulia Yusrini DjabirDewita FatiahMuhammad Rasul PratamaTenri Zulfa Ayu Dwi PutriRizkya ChaeratunnisaNadila Pratiwi LatadaMukarram MudjahidRangga Meidianto AsriFirzan NainuPublished in: ACS omega (2024)
This study delved into the consequences of prolonged administration of vitamin D 3 on innate immune systems, particularly NF-κB and JAK/STAT, in Drosophila melanogaster . The outcomes indicated that vitamin D 3 treatment exhibited a notable capacity to improve the survival of adult flies with compromised immune functions, a condition induced by the loss of PGRP-LB, particularly when the flies were exposed to heat-killed Escherichia coli . The PGRP-LB Δ mutant line that was treated with heat-killed E. coli experienced reduced survival. Treatment of heat-killed E. coli -treated PGRP-LB Δ with vitamin D 3 resulted in improved survival, and this phenotypic feature might be due to the downregulation of gene expression in the NF-κB and JAK/STAT pathways. However, a higher concentration of vitamin D 3 was associated with decreased survival, potentially linked to intricate immunological responses. The research also underscored the influence of vitamin D 3 on the expression of antioxidant genes, sod1 and sod2 , indicating an augmented resistance to oxidative stress. Further, this study revealed the effect of vitamin D 3 on the reproductive status of the autoinflammatory model, showing an increase in pupae and adult flies with a treatment of 10 mM vitamin D 3 , suggesting the potential benefits of vitamin D 3 on the reproductive profile. Overall, this study provides preliminary insights into the complex interactions between vitamin D 3 , immune pathways, oxidative responses in the cell, and reproduction in Drosophila .
Keyphrases
- drosophila melanogaster
- oxidative stress
- escherichia coli
- signaling pathway
- gene expression
- pi k akt
- stem cells
- type diabetes
- cell proliferation
- lps induced
- genome wide
- free survival
- cystic fibrosis
- poor prognosis
- single cell
- dna damage
- combination therapy
- transcription factor
- risk assessment
- ischemia reperfusion injury
- biofilm formation
- bone marrow
- nuclear factor
- insulin resistance
- klebsiella pneumoniae
- binding protein
- glycemic control