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Mechanistic model of CF‐related cholangiopathy. The absence of apical CFTR triggers abnormal permeability and a pre‐inflammatory status both in cholangiocytes and enterocytes. The genetic background promotes an ill‐adapted response to gut‐derived pathobiont, which is aggravated by diet‐induced dysbiosis. The combined failure of CFTR‐deficient cholangiocytes and host immunity in this response leads to bile duct damage.
