Anti-interleukin-6 receptor antibody treatment ameliorates postoperative adhesion formation.
Animals
Antibodies, Monoclonal
/ immunology
Ascitic Fluid
/ chemistry
Humans
Interleukin-6
/ analysis
Mice
Mice, Inbred C57BL
Myofibroblasts
/ metabolism
Neutrophils
/ metabolism
Postoperative Complications
/ prevention & control
Receptors, Interleukin-6
/ immunology
Tissue Adhesions
/ prevention & control
Transforming Growth Factor beta1
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
26 11 2019
26 11 2019
Historique:
received:
30
05
2019
accepted:
05
11
2019
entrez:
28
11
2019
pubmed:
28
11
2019
medline:
11
11
2020
Statut:
epublish
Résumé
Postoperative adhesion formation often ruins the quality of life or is an obstacle to illnesses with curative operation such as cancer. Previously we demonstrated that interferon-γ-promoted fibrin deposition drove postoperative adhesion formation. However, its underlying cellular and molecular mechanisms remain poorly understood. We found that myofibroblasts of the adhesion predominantly expressed signature molecules of mesothelial cells that line the serosa. Microarray analysis revealed IL-6 as a key underlying player, supported by elevated IL-6 levels in the peritoneal fluid of post-laparotomy human subjects. Injured serosa of cecum-cauterized mice also exhibited induction of Il6, which was followed by Tnf, concomitant with rapid accumulation of neutrophils, substantial population of which expressed TGF-β1, a master regulator of fibrosis. Besides, neutrophil-ablated mice showed reduction in induction of the adhesion, suggesting that TGF-β1
Identifiants
pubmed: 31772282
doi: 10.1038/s41598-019-54175-1
pii: 10.1038/s41598-019-54175-1
pmc: PMC6879753
doi:
Substances chimiques
Antibodies, Monoclonal
0
Interleukin-6
0
Receptors, Interleukin-6
0
Transforming Growth Factor beta1
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17558Références
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