2018
DOI: 10.18632/aging.101610
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Abstract: High glucose levels negatively affect immune response. However, the underlying mechanisms are not well understood. Upon infection, the round worm C. elegans induces multiple gene transcription programs, including the Nrf2/SKN-1-mediated detoxification program, to activate the innate immunity. In this study, we find that high glucose conditions inhibit the SKN-1-mediated immune response to Salmonella typhimurium, exacerbate the infection and greatly decrease survival. The effect of glucose shows specificity to … Show more

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Cited by 12 publications
(9 citation statements)
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References 46 publications
(65 reference statements)
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“…The correlation observed between the decreased mRNA levels of skn-1 and two of their transcriptional targets in glucose-treated worms surely warrants a further in-depth study. A similar downregulation of gcs-1 and gst-4 mRNA has been reported in glucose-fed worms, which was shown to be a consequence of the inhibition of the SKN-1-mediated immune response to the infection with Salmonella typhimurium [69]. Along the same lines, the SKN-1-mediated increase of expression of gcs-1 and gst-4 in response to Paraquat was suppressed in the presence of glucose [70].…”
Section: Discussionsupporting
confidence: 57%
“…The correlation observed between the decreased mRNA levels of skn-1 and two of their transcriptional targets in glucose-treated worms surely warrants a further in-depth study. A similar downregulation of gcs-1 and gst-4 mRNA has been reported in glucose-fed worms, which was shown to be a consequence of the inhibition of the SKN-1-mediated immune response to the infection with Salmonella typhimurium [69]. Along the same lines, the SKN-1-mediated increase of expression of gcs-1 and gst-4 in response to Paraquat was suppressed in the presence of glucose [70].…”
Section: Discussionsupporting
confidence: 57%
“…Gene expression levels were normalized to actin ( ACT1 ) and expressed as fold changes to that of the wild-type. Primers have been published before [14], which are also listed in Supplementary Information, Supplementary Table 2.…”
Section: Methodsmentioning
confidence: 99%
“…Similarly, high glucose can robustly increase the mortality rate and shorten lifespan [1113]. High glucose uptake compromises the innate immune response to infection in C. elegans [14]. RNA sequencing in C. elegans demonstrates that in response to glucose, conserved genetic programs are induced to modulate several biological processes [15].…”
Section: Introductionmentioning
confidence: 99%
“…If it is required for mitochondrial functioning, UPR mt is triggered to actively promote the repair and recovery of mitochondrial function and integrity. In Caenorhabditis elegans , the UPR mt is monitored primarily by the stress activated transcription factor ATFS-1 (of the basic-region leucine zipper family), as well by SKN-1 (skinhead-1, sharing an orthologous homology with Nrf1 and Nrf2) (55,56). The mammalian UPR mt is regulated by ATF5-mediated expression of several mitochondrial chaperone and protease genes to promote its OXPHOS and cell growth during mitochondrial dysfunction (57).…”
Section: Resultsmentioning
confidence: 99%