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- W4313373471 abstract "Abstract HLA-B27, which predisposes to spondyloarthritis (SpA), can misfold, generate endoplasmic reticulum stress, and activate the unfolded protein response (UPR). The UPR may contribute to SpA pathogenesis by promoting pro-inflammatory cytokine production. CHOP, which is upregulated by the PERK arm of the UPR, is required for excess IL-23 production during UPR-TLR co-activation. Here, we examined whether CHOP deficiency in HLA-B27-transgenic (B27+) rats affects pro-inflammatory cytokine production and gut inflammation. CHOP-deficient (CHOP-) Lewis rats were generated using CRISPR/CAS9 editing and crossed with B27+ Lewis animals to create B27+CHOP− rats. CHOP expression was not detectable by western blot in CHOP− cells when treated with thapsigargin, to induce UPR and CHOP expression. In contrast to CHOP+ macrophages, CHOP-cells did not express Il23a upon UPR-TLR co-activation. Histological scoring of colon samples from 6-month-old animals showed a trend to increased inflammation in B27+CHOP− compared to B27+CHOP+ rats (8.05±1.11 vs 6.87±1.40; p=0.07). B27-CHOP− rats had no gut inflammation similar to B27-CHOP+ WT rats (scores ≤ 2). RNASeq analysis of colon tissue showed significantly increased expression of 73 genes in B27+CHOP− vs B27+CHOP+ rats, including pro-inflammatory genes like Il1a, Tnf, and Il4r. TOPPGENE analysis revealed that the differentially expressed genes are involved in processes like inflammation, IL-6 production and cytokine secretion. Our data demonstrate that CHOP depletion does not prevent SpA development, but rather it may exacerbate gut inflammation. This suggests that CHOP may play a protective role in HLA-B27 associated disease. This axis warrants further investigation as a therapeutic avenue." @default.
- W4313373471 created "2023-01-06" @default.
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- W4313373471 date "2020-05-01" @default.
- W4313373471 modified "2023-09-27" @default.
- W4313373471 title "CHOP depletion does not prevent gut inflammation in experimental spondyloarthritis" @default.
- W4313373471 doi "https://doi.org/10.4049/jimmunol.204.supp.237.4" @default.
- W4313373471 hasPublicationYear "2020" @default.
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