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Obesity Exacerbates Lupus Activity in Fc Gamma Receptor IIb Deficient Lupus Mice Partly through Saturated Fatty Acid-Induced Gut Barrier Defect and Systemic Inflammation.

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  • Additional Information
    • Source:
      Publisher: Karger Country of Publication: Switzerland NLM ID: 101469471 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1662-8128 (Electronic) Linking ISSN: 1662811X NLM ISO Abbreviation: J Innate Immun Subsets: MEDLINE
    • Publication Information:
      Original Publication: Basel, Switzerland : Karger, c2009-
    • Subject Terms:
      Lipopolysaccharides* ; Fatty Acids*; Mice ; Female ; Animals ; Cytokines ; Inflammation ; Obesity ; Interleukin-6 ; Mice, Inbred C57BL
    • Abstract:
      The prevalence of obesity is increasing, and the coexistence of obesity and systemic lupus erythematosus (lupus) is possible. A high-fat diet (HFD) was orally administered for 6 months in female 8-week-old Fc gamma receptor IIb deficient (FcgRIIb-/-) lupus or age and gender-matched wild-type (WT) mice. Lupus nephritis (anti-dsDNA, proteinuria, and increased creatinine), gut barrier defect (fluorescein isothiocyanate dextran), serum lipopolysaccharide (LPS), serum interleukin (IL)-6, liver injury (alanine transaminase), organ fibrosis (liver and kidney pathology), spleen apoptosis (activated caspase 3), and aorta thickness (but not weight gain and lipid profiles) were more prominent in HFD-administered FcgRIIb-/- mice than the obese WT, without injury in regular diet-administered mice (both FcgRIIb-/- and WT). In parallel, combined palmitic acid (PA; a saturated fatty acid) with LPS (PA + LPS) induced higher tumor necrotic factor-α, IL-6, and IL-10 in the supernatant, inflammatory genes (inducible nitric oxide synthase and IL-1β), reactive oxygen species (dihydroethidium), and glycolysis with reduced mitochondrial activity (extracellular flux analysis) when compared with the activation by each molecule alone in both FcgRIIb-/- and WT macrophages. However, the alterations of these parameters were more prominent in PA + LPS-administered FcgRIIb-/- than in the WT cells. In conclusion, obesity accelerated inflammation in FcgRIIb-/- mice, partly due to the more potent responses from the loss of inhibitory FcgRIIb against PA + LPS with obesity-induced gut barrier defect.
      (© 2022 The Author(s). Published by S. Karger AG, Basel.)
    • Contributed Indexing:
      Keywords: Gut barrier defect; High-fat diet; Lupus; Obesity; Systemic inflammation
    • Accession Number:
      0 (Lipopolysaccharides)
      0 (Fc gamma receptor IIB)
      0 (Fatty Acids)
      0 (Cytokines)
      0 (Interleukin-6)
    • Publication Date:
      Date Created: 20221011 Date Completed: 20231226 Latest Revision: 20250605
    • Publication Date:
      20250605
    • Accession Number:
      PMC10643905
    • Accession Number:
      10.1159/000526206
    • Accession Number:
      36219976