ArticleScientific reports2025
HFD-induced LPS translocation and elevated blood lipids exacerbated the inflammatory response in allergic rhinitis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Inhibition of adipocyte-macrophage interaction via CSF1-CSF1R by curcumin.Journal of physiology and biochemistry · 2026Article
- Plasticity of the infant immune system during the perinatal period.Nature reviews. Immunology · 2026Review
- Mechanistic insights into natural product-driven modulation of NLRP3-inflammasome signalling in metabolic syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Gut microbiota as a therapeutic target of Chinese herbal medicine in allergic rhinitis: the gut-nasal axis and immunity.Frontiers in physiology · 2026Review
- Multi-omics insights into dietary zinc-mediated reprogramming of the gut-nasal ecosystem in allergic rhinitis.Frontiers in allergy · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
Allergic rhinitis (AR) is one of the most prevalent chronic diseases, with studies indicating that a high-fat diet (HFD) may heighten susceptibility to AR. This study aims to investigate the impact of HFD on ovalbumin (OVA)-induced AR using both an OVA-sensitized rat model and a macrophage model treated with palmitic acid (PA). The systemic effects of HFD were explored with respect to intestinal barrier integrity, serum lipids and lipopolysaccharide (LPS) levels, and inflammatory response. In AR rats fed with HFD, there was a reduction in the expression of tight junction proteins in colon tissues, increased serum levels of lipids and LPS, and elevated inflammatory responses in both nasal lavage fluid (NLF) and serum. Additionally, there was enhanced NF-κB and NLRP3 inflammasome activity observed in both nasal and colon tissues. In vitro experiments demonstrated that PA and LPS synergistically amplified inflammatory responses in THP-1-derived macrophages, paralleling the systemic findings. These results suggest that HFD-induced intestinal barrier dysfunction facilitates the translocation of LPS into the bloodstream. Elevated serum LPS level, together with increased blood lipids levels, may exacerbate the inflammatory response in AR through the activation of NF-κB and NLRP3 inflammasome.
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