AI Article Synopsis
- The study focuses on the lesser-known effects of lupus on the intestines and liver, highlighting the importance of gut-liver interactions.
- Researchers conducted experiments on C57BL/6 mice with induced lupus, measuring fecal calprotectin levels and assessing various inflammatory and protein biomarkers over six weeks.
- Findings revealed an early increase in fecal calprotectin and significant liver inflammation, marking the activation of specific signaling pathways related to lupus progression.
Article Abstract
Background: Intestinal and hepatic manifestations of lupus seem to be underestimated in comparison to other major organ lesions. Although recent data point to gut-liver axis involvement in lupus, gut permeability dysfunction and liver inflammation need to be more investigated.
Objective: This study aims to assess fecal calprotectin, intestinal tight junction proteins and liver inflammation pathway in wild-type murine imiquimod- induced lupus.
Methods: C57BL/6 mice were topically treated on their right ears with 1.25 mg of 5% imiquimod cream, three times per week for six weeks. Fecal calprotectin was collected at day 0, 22 and 45. Renal, liver and intestinal pathology, as well as inflammatory markers, intestinal tight junction proteins, and protein in liver were assessed at sacrifice.
Results: At six weeks, lupus nephritis was confirmed on histopathology and NGAL and KIM-1 expression. Calprotectin rise started at day 22 and persists at day 45. Protein expression of Claudine, ZO-1 and occludin was significantly decreased. protein was significantly increased in liver with necro-inflammation and increased TLR4, TLR7, and pNFκB/NFκB liver expression.
Conclusion: This study is the first to demonstrate early fecal calprotectin increase and liver activation of TLR4- NFκB pathway in wild-type murine imiquimod-induced lupus.
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| http://dx.doi.org/10.1177/0961203321995254 | DOI Listing |
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