Gut microbiota facilitate chronic spontaneous urticaria.
Lei ZhuXingxing JianBingjing ZhouRunqiu LiuMelba MuñozWan SunLu XieXiang ChenCong PengMarcus MaurerRunqiu LiuPublished in: Nature communications (2024)
Chronic spontaneous urticaria (CSU) comes with gut dysbiosis, but its relevance remains elusive. Here we use metagenomics sequencing and short-chain fatty acids metabolomics and assess the effects of human CSU fecal microbial transplantation, Klebsiella pneumoniae, Roseburia hominis, and metabolites in vivo. CSU gut microbiota displays low diversity and short-chain fatty acids production, but high gut Klebsiella pneumoniae levels, negatively correlates with blood short-chain fatty acids levels and links to high disease activity. Blood lipopolysaccharide levels are elevated, link to rapid disease relapse, and high gut levels of conditional pathogenic bacteria. CSU microbiome transfer and Klebsiella pneumoniae transplantation facilitate IgE-mediated mast cell(MC)-driven skin inflammatory responses and increase intestinal permeability and blood lipopolysaccharide accumulation in recipient mice. Transplantation of Roseburia hominis and caproate administration protect recipient mice from MC-driven skin inflammation. Here, we show gut microbiome alterations, in CSU, may reduce short-chain fatty acids and increase lipopolysaccharide levels, respectively, and facilitate MC-driven skin inflammation.
Keyphrases
- klebsiella pneumoniae
- fatty acid
- multidrug resistant
- escherichia coli
- disease activity
- oxidative stress
- endothelial cells
- inflammatory response
- rheumatoid arthritis
- soft tissue
- lps induced
- mass spectrometry
- cell therapy
- rheumatoid arthritis patients
- ms ms
- single cell
- wound healing
- type diabetes
- ankylosing spondylitis
- immune response
- microbial community
- mesenchymal stem cells
- quantum dots
- bone marrow
- insulin resistance
- sensitive detection