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Peer-reviewedCC BYJournal of Crohn's & colitis

B cell/adipocyte crosstalk amplifies MCP-1 secretion, M2-like macrophage accumulation, and polarization in gut-associated, inflamed adipose tissue.

  • Marie Christine Goess1,2
  • Julia M Heinze1,2
  • Julian Hofmann3
  • Annalisa Buck4,5
  • Iana Gadjalova1,2
  • Marie-Christin Weber4
  • Sandra Ring1,2
  • Joerg M Buescher6
  • Matteo Villa7
  • Philipp-Alexander Neumann4,5
  • Jürgen Ruland1,2,8,9,10
  • Selina J Keppler1,2,7
10 affiliations
  1. 1Institute of Laboratory Medicine, School of Medicine and Health, TUM University Hospital, Munich, Germany.
  2. 2TranslaTUM, Central Institute for Translational Cancer Research, Munich, Germany.
  3. 3Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
  4. 4Department of Surgery, Technical University of Munich, School of Medicine and Health, Munich, Germany.
  5. 5Institute for Advanced Study, Technical University of Munich, Munich, Germany.
  6. 6Max Planck Institute for Immunobiology and Epigenetics, Freiburg 79108, Germany.
  7. 7Division of Rheumatology and Immunology, Medical University Graz, Graz, Austria.
  8. 8German Cancer Consortium (DKTK), partner site Munich, a partnership between DKFZ, TUM University Hospital, Munich, Germany.
  9. 9German Center for Infection Research (DZIF), partner side Munich, Munich, Germany.
  10. 10German Center for Child and Adolescent Health (DZKJ), partner side Munich, Munich, Germany.
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Abstract

During Crohn's disease (CD), hyperplasia of the mesenteric white adipose tissue (WAT), called creeping fat (CrF), is associated with the accumulation of immune cells. Here we investigated the impact of B cell/adipocyte crosstalk on immune cell recruitment and inflammation within inflammatory bowel disease-related adipose tissue. We used flow cytometry and in vitro 3D culture systems of biopsies from CrF of CD patients as well as a mouse model of intestinal inflammation, in vitro co-cultures, mass spectrometry, and single-cell RNA sequencing to evaluate the impact of B cell/adipocyte interplay on monocyte chemoattractant protein-1 (MCP-1) production and macrophage polarization. Employing primary human and mouse 3D adipocyte cultures, we observed that adipocytes from CD patients displayed a persistent inflammatory phenotype even after prolonged time in culture, a cytokine secretion profile also recapitulated via lipopolysaccharide stimulation. Analyzing CrF of CD patients as well as WAT of a mouse model of intestinal inflammation, we found an accumulation of B cells. B cell/adipocyte co-cultures led to elevated secretion of MCP-1 by primary adipocytes, facilitating macrophage migration. Consequently, co-transfer of B cells with T cells increased T cell activation and M2-like macrophage accumulation in inflamed mouse WAT. Mass spectrometry and single-cell RNA sequencing analyses suggested that the B cell/adipocyte crosstalk establishes a microenvironment that may promote M2-like macrophage polarization. B cell/adipocyte interactions in CD-associated inflamed adipose tissue increase MCP-1 and lactate, promoting recruitment and M2-like polarization of macrophages, likely amplifying local WAT inflammation.

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Cite

BibTeXRIS
BibTeX
@article{goess2026celladipocyte,
  title = {{B cell/adipocyte crosstalk amplifies MCP-1 secretion, M2-like macrophage accumulation, and polarization in gut-associated, inflamed adipose tissue.}},
  author = {Marie Christine Goess and Julia M Heinze and Julian Hofmann and Annalisa Buck and Iana Gadjalova and Marie-Christin Weber and Sandra Ring and Joerg M Buescher and Matteo Villa and Philipp-Alexander Neumann and Jürgen Ruland and Selina J Keppler},
  journal = {Journal of Crohn's \& colitis},
  year = {2026},
  month = nov,
  doi = {10.1093/ecco-jcc/jjag182},
  url = {https://europepmc.org/article/MED/42998367},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - B cell/adipocyte crosstalk amplifies MCP-1 secretion, M2-like macrophage accumulation, and polarization in gut-associated, inflamed adipose tissue.
AU  - Marie Christine Goess
AU  - Julia M Heinze
AU  - Julian Hofmann
AU  - Annalisa Buck
AU  - Iana Gadjalova
AU  - Marie-Christin Weber
AU  - Sandra Ring
AU  - Joerg M Buescher
AU  - Matteo Villa
AU  - Philipp-Alexander Neumann
AU  - Jürgen Ruland
AU  - Selina J Keppler
PY  - 2026
DA  - 2026/11/01
JO  - Journal of Crohn's & colitis
DO  - 10.1093/ecco-jcc/jjag182
UR  - https://europepmc.org/article/MED/42998367
AB  - During Crohn's disease (CD), hyperplasia of the mesenteric white adipose tissue (WAT), called creeping fat (CrF), is associated with the accumulation of immune cells. Here we investigated the impact of B cell/adipocyte crosstalk on immune cell recruitment and inflammation within inflammatory bowel disease-related adipose tissue. We used flow cytometry and in vitro 3D culture systems of biopsies from CrF of CD patients as well as a mouse model of intestinal inflammation, in vitro co-cultures, mass spectrometry, and single-cell RNA sequencing to evaluate the impact of B cell/adipocyte interplay on monocyte chemoattractant protein-1 (MCP-1) production and macrophage polarization. Employing primary human and mouse 3D adipocyte cultures, we observed that adipocytes from CD patients displayed a persistent inflammatory phenotype even after prolonged time in culture, a cytokine secretion profile also recapitulated via lipopolysaccharide stimulation. Analyzing CrF of CD patients as well as WAT of a mouse model of intestinal inflammation, we found an accumulation of B cells. B cell/adipocyte co-cultures led to elevated secretion of MCP-1 by primary adipocytes, facilitating macrophage migration. Consequently, co-transfer of B cells with T cells increased T cell activation and M2-like macrophage accumulation in inflamed mouse WAT. Mass spectrometry and single-cell RNA sequencing analyses suggested that the B cell/adipocyte crosstalk establishes a microenvironment that may promote M2-like macrophage polarization. B cell/adipocyte interactions in CD-associated inflamed adipose tissue increase MCP-1 and lactate, promoting recruitment and M2-like polarization of macrophages, likely amplifying local WAT inflammation.
SN  - 1873-9946
SN  - 1876-4479
ER  -