Intercellular interaction between FAP+ fibroblasts and
CD150+inflammatory monocytes mediates fibrostenosis in Crohn's
disease

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Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates ...

Přehled o publikaci

J 2024

Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease

KE, Bo-Jun, Saeed ABDURAHIMAN, Francesca BISCU, Gaia ZANELLA, Gabriele DRAGONI et. al.

Basic information

Original name

Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease

Authors

Edition

Journal of Clinical Investigation, Ann Arbor, AMER SOC CLINICAL INVESTIGATION INC, 2024, 0021-9738

Other information

Language

English

Type of outcome

Article in a journal

Country of publisher

United States of America

Confidentiality degree

is not subject to a state or trade secret

References:

URL

Organization

Lékařská fakulta – Repository – Repository

DOI

http://dx.doi.org/10.1172/JCI173835

UT WoS

001307280000026

EID Scopus

2-s2.0-85201438461

Keywords in English

Crohn's disease; FAP+ fibroblasts; CD150+inflammatory monocytes

Links

LX22NPO5107, research and development project.

Changed: 2/10/2024 00:50, RNDr. Daniel Jakubík

Abstract

V originále

Crohn's disease (CD) is marked by recurring intestinal inflammation and tissue injury, often resulting in fibrostenosis and bowel obstruction, necessitating surgical intervention with high recurrence rates. To elucidate the mechanisms underlying fibrostenosis in CD, we analyzed the transcriptome of cells isolated from the transmural ileum of patients with CD, including a trio of lesions from each patient: non-affected, inflamed, and stenotic ileum samples, and compared them with samples from patients without CD. Our computational analysis revealed that profibrotic signals from a subset of monocyte-derived cells expressing CD150 induced a disease-specific fibroblast population, resulting in chronic inflammation and tissue fibrosis. The transcription factor TWIST1 was identified as a key modulator of fibroblast activation and extracellular matrix (ECM) deposition. Genetic and pharmacological inhibition of TWIST1 prevents fibroblast activation, reducing ECM production and collagen deposition. Our findings suggest that the myeloid-stromal axis may offer a promising therapeutic target to prevent fibrostenosis in CD.

Files attached

https://is.muni.cz/publication/2438977/Intercellular_interaction_between_FAP__fibroblasts_and_CD150_inflammatory_monocytes_mediates_fibrostenosis_in_Crohn_s_disease.pdf

Cite

KE, Bo-Jun, Saeed ABDURAHIMAN, Francesca BISCU, Gaia ZANELLA, Gabriele DRAGONI, Sneha SANTHOSH, De Simone VERONICA, Anissa ZOUZAF, van Baarle LIES, Michelle STAKENBORG, Veronika BOSÁKOVÁ, Van Rymenant YENTL, Emile VERHULST, Sare VERSTOCKT, Elliott KLEIN, Gabriele BISLENGHI, Albert WOLTHUIS, Jan FRIČ, Christine BREYNAERT, Andre D'HOORE, van der Veken PIETER, De Meester INGRID, Sara LOVISA, Lukas J A C HAWINKELS, Bram VERSTOCKT, De Hertogh GERT, Severine VERMEIRE and Gianluca MATTEOLI. Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease. Journal of Clinical Investigation. Ann Arbor: AMER SOC CLINICAL INVESTIGATION INC, 2024, vol. 134, No 16, p. 1-19. ISSN 0021-9738. Available from: https://dx.doi.org/10.1172/JCI173835.

@article{64208,
   author = {Ke, BoandJun and Abdurahiman, Saeed and Biscu, Francesca and Zanella, Gaia and Dragoni, Gabriele and Santhosh, Sneha and Veronica, De Simone and Zouzaf, Anissa and Lies, van Baarle and Stakenborg, Michelle and Bosáková, Veronika and Yentl, Van Rymenant and Verhulst, Emile and Verstockt, Sare and Klein, Elliott and Bislenghi, Gabriele and Wolthuis, Albert and Frič, Jan and Breynaert, Christine and D'Hoore, Andre and Pieter, van der Veken and Ingrid, De Meester and Lovisa, Sara and Hawinkels, Lukas J A C and Verstockt, Bram and Gert, De Hertogh and Vermeire, Severine and Matteoli, Gianluca},
   article_location = {Ann Arbor},
   article_number = {16},
   doi = {http://dx.doi.org/10.1172/JCI173835},
   keywords = {Crohn's disease; FAP+ fibroblasts; CD150+inflammatory monocytes},
   language = {eng},
   issn = {0021-9738},
   journal = {Journal of Clinical Investigation},
   title = {Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease},
   url = {https://www.jci.org/articles/view/173835},
   volume = {134},
   year = {2024}
}

TY  - JOUR
ID  - 64208
AU  - Ke, Bo-Jun - Abdurahiman, Saeed - Biscu, Francesca - Zanella, Gaia - Dragoni, Gabriele - Santhosh, Sneha - Veronica, De Simone - Zouzaf, Anissa - Lies, van Baarle - Stakenborg, Michelle - Bosáková, Veronika - Yentl, Van Rymenant - Verhulst, Emile - Verstockt, Sare - Klein, Elliott - Bislenghi, Gabriele - Wolthuis, Albert - Frič, Jan - Breynaert, Christine - D'Hoore, Andre - Pieter, van der Veken - Ingrid, De Meester - Lovisa, Sara - Hawinkels, Lukas J A C - Verstockt, Bram - Gert, De Hertogh - Vermeire, Severine - Matteoli, Gianluca
PY  - 2024
TI  - Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease
JF  - Journal of Clinical Investigation
VL  - 134
IS  - 16
SP  - 1-19
EP  - 1-19
PB  - AMER SOC CLINICAL INVESTIGATION INC
SN  - 0021-9738
KW  - Crohn's disease
KW  - FAP+ fibroblasts
KW  - CD150+inflammatory monocytes
UR  - https://www.jci.org/articles/view/173835
N2  - Crohn's disease (CD) is marked by recurring intestinal inflammation and tissue injury, often resulting in fibrostenosis and bowel obstruction, necessitating surgical intervention with high recurrence rates. To elucidate the mechanisms underlying fibrostenosis in CD, we analyzed the transcriptome of cells isolated from the transmural ileum of patients with CD, including a trio of lesions from each patient: non-affected, inflamed, and stenotic ileum samples, and compared them with samples from patients without CD. Our computational analysis revealed that profibrotic signals from a subset of monocyte-derived cells expressing CD150 induced a disease-specific fibroblast population, resulting in chronic inflammation and tissue fibrosis. The transcription factor TWIST1 was identified as a key modulator of fibroblast activation and extracellular matrix (ECM) deposition. Genetic and pharmacological inhibition of TWIST1 prevents fibroblast activation, reducing ECM production and collagen deposition. Our findings suggest that the myeloid-stromal axis may offer a promising therapeutic target to prevent fibrostenosis in CD.
ER  -

KE, Bo-Jun, Saeed ABDURAHIMAN, Francesca BISCU, Gaia ZANELLA, Gabriele DRAGONI, Sneha SANTHOSH, De Simone VERONICA, Anissa ZOUZAF, van Baarle LIES, Michelle STAKENBORG, Veronika BOSÁKOVÁ, Van Rymenant YENTL, Emile VERHULST, Sare VERSTOCKT, Elliott KLEIN, Gabriele BISLENGHI, Albert WOLTHUIS, Jan FRIČ, Christine BREYNAERT, Andre D'HOORE, van der Veken PIETER, De Meester INGRID, Sara LOVISA, Lukas J A C HAWINKELS, Bram VERSTOCKT, De Hertogh GERT, Severine VERMEIRE and Gianluca MATTEOLI. Intercellular interaction between FAP+ fibroblasts and CD150+inflammatory monocytes mediates fibrostenosis in Crohn's disease. \textit{Journal of Clinical Investigation}. Ann Arbor: AMER SOC CLINICAL INVESTIGATION INC, 2024, vol.~134, No~16, p.~1-19. ISSN~0021-9738. Available from: https://dx.doi.org/10.1172/JCI173835.