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10.1136/gutjnl-2015-310847

http://scihub22266oqcxt.onion/10.1136/gutjnl-2015-310847
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C5595104!5595104!27371534
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suck abstract from ncbi


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pmid27371534      Gut 2017 ; 66 (10): 1748-60
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  • Hemidesmosome integrity protects the colon against colitis and colorectal cancer #MMPMID27371534
  • De Arcangelis A; Hamade H; Alpy F; Normand S; Bruyère E; Lefebvre O; Méchine-Neuville A; Siebert S; Pfister V; Lepage P; Laquerriere P; Dembele D; Delanoye-Crespin A; Rodius S; Robine S; Kedinger M; Van Seuningen I; Simon-Assmann P; Chamaillard M; Labouesse M; Georges-Labouesse E
  • Gut 2017[Oct]; 66 (10): 1748-60 PMID27371534show ga
  • Objective: Epidemiological and clinical data indicate that patients suffering from IBD with long-standing colitis display a higher risk to develop colorectal high-grade dysplasia. Whereas carcinoma invasion and metastasis rely on basement membrane (BM) disruption, experimental evidence is lacking regarding the potential contribution of epithelial cell/BM anchorage on inflammation onset and subsequent neoplastic transformation of inflammatory lesions. Herein, we analyse the role of the ?6?4 integrin receptor found in hemidesmosomes that attach intestinal epithelial cells (IECs) to the laminin-containing BM. Design: We developed new mouse models inducing IEC-specific ablation of ?6 integrin either during development (?6?IEC) or in adults (?6?IEC-TAM). Results: Strikingly, all ?6?IEC mutant mice spontaneously developed long-standing colitis, which degenerated overtime into infiltrating adenocarcinoma. The sequence of events leading to disease onset entails hemidesmosome disruption, BM detachment, IL-18 overproduction by IECs, hyperplasia and enhanced intestinal permeability. Likewise, IEC-specific ablation of ?6 integrin induced in adult mice (?6?IEC-TAM) resulted in fully penetrant colitis and tumour progression. Whereas broad-spectrum antibiotic treatment lowered tissue pathology and IL-1? secretion from infiltrating myeloid cells, it failed to reduce Th1 and Th17 response. Interestingly, while the initial intestinal inflammation occurred independently of the adaptive immune system, tumourigenesis required B and T lymphocyte activation. Conclusions: We provide for the first time evidence that loss of IECs/BM interactions triggered by hemidesmosome disruption initiates the development of inflammatory lesions that progress into high-grade dysplasia and carcinoma. Colorectal neoplasia in our mouse models resemble that seen in patients with IBD, making them highly attractive for discovering more efficient therapies.
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