β7-Integrin worsens diet-induced metabolic syndrome in mice by altering intestinal lipid handling and colonic inflammatory monocyte infiltration
Abstract
Western diet (WD)-induced metabolic syndrome (MetS) involves obesity, insulin resistance, dyslipidemia, and low-grade inflammation. While β7 integrin-expressing adaptive immune cells contribute to WD-induced MetS, the role of β7 integrin in innate immunity remains unclear. To address this, the effect of antibody-mediated β7 integrin blockade or β7 integrin deficiency on WD-induced MetS was studied in recombination activating gene-2-deficient mice. Loss or inhibition of β7 integrin protected mice from WD-induced obesity, dyslipidemia, and glucose intolerance, partially via loss of β7 integrin-MAdCAM-1 interactions. β7 integrin deficiency altered intestinal lipid handling and monocyte infiltration into the colon and adipose tissue. Adoptive transfer confirmed that β7-expressing monocytes promote metabolic dysfunction in WD-fed recipients. Phospho-signaling analyses revealed attenuated PI3K-Akt pathway activation in β7 integrin-deficient colonic macrophages, and antibody treatments caused minor shifts in fecal microbiota profiles. Thus, β7 integrin-expressing innate immune cells drive WD-induced metabolic inflammation through monocyte recruitment, macrophage activation, and altered intestinal fat metabolism.
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BibTeX
@article{eswaran2026β7integrin,
title = {{β7-Integrin worsens diet-induced metabolic syndrome in mice by altering intestinal lipid handling and colonic inflammatory monocyte infiltration}},
author = {Sreepradha Eswaran and Agnes Seeger and Sabine Hamm and Kerstin Scheuer and Nicole Treichel and Juliane Hermann and Trong-Hieu Nguyen and Thomas Clavel and Joachim Jankowski and Norbert Wagner and Angela Schippers},
journal = {iScience},
year = {2026},
month = oct,
doi = {10.1016/j.isci.2026.118042},
url = {https://www.cell.com/iscience/fulltext/S2589-0042(26)03425-5},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - β7-Integrin worsens diet-induced metabolic syndrome in mice by altering intestinal lipid handling and colonic inflammatory monocyte infiltration
AU - Sreepradha Eswaran
AU - Agnes Seeger
AU - Sabine Hamm
AU - Kerstin Scheuer
AU - Nicole Treichel
AU - Juliane Hermann
AU - Trong-Hieu Nguyen
AU - Thomas Clavel
AU - Joachim Jankowski
AU - Norbert Wagner
AU - Angela Schippers
PY - 2026
DA - 2026/10/27
JO - iScience
DO - 10.1016/j.isci.2026.118042
UR - https://www.cell.com/iscience/fulltext/S2589-0042(26)03425-5
AB - Western diet (WD)-induced metabolic syndrome (MetS) involves obesity, insulin resistance, dyslipidemia, and low-grade inflammation. While β7 integrin-expressing adaptive immune cells contribute to WD-induced MetS, the role of β7 integrin in innate immunity remains unclear. To address this, the effect of antibody-mediated β7 integrin blockade or β7 integrin deficiency on WD-induced MetS was studied in recombination activating gene-2-deficient mice. Loss or inhibition of β7 integrin protected mice from WD-induced obesity, dyslipidemia, and glucose intolerance, partially via loss of β7 integrin-MAdCAM-1 interactions. β7 integrin deficiency altered intestinal lipid handling and monocyte infiltration into the colon and adipose tissue. Adoptive transfer confirmed that β7-expressing monocytes promote metabolic dysfunction in WD-fed recipients. Phospho-signaling analyses revealed attenuated PI3K-Akt pathway activation in β7 integrin-deficient colonic macrophages, and antibody treatments caused minor shifts in fecal microbiota profiles. Thus, β7 integrin-expressing innate immune cells drive WD-induced metabolic inflammation through monocyte recruitment, macrophage activation, and altered intestinal fat metabolism.
SN - 2589-0042
ER -