title: Oral administration of Bifidobacterium longum CECT 7347 ameliorates gliadin-induced alterations in liver iron mobilisation.
abstract: Coeliac disease is an autoimmune disorder triggered by gluten intake, causing intestinal inflammation and mucosal damage commonly associated with the malabsorption of nutrients and ferropenic anaemia. The present study evaluates the effects of the oral administration of Bifidobacterium longum CECT 7347 on gliadin-mediated alterations in hepatic Fe deposition and Hb concentration, liver transferrin receptor (TfR)-2, IL-6, TNF-α and hepcidin (Hamp) expression (mRNA), and active hepcidin peptide production by liquid chromatography–MS/MS. Weanling rats, sensitised or not with interferon (IFN)-γ, were fed with gliadins and/or the bifidobacterial strain. Gliadin feeding increased hepatic Fe deposition; however, only gliadin-fed sensitised animals showed lower Hb concentrations than the controls. TfR2 expression decreased after gliadins were fed to both sensitised and non-sensitised animals,and restored by the administration of B. longum. These observations were accompanied by increases in IL-6 expression levels in all the treatment groups; however, TNF-α expression only increased significantly in animals fed gliadins alone or together with B. longum if they had previously been sensitised with IFN-γ. Liver expression levels of Hamp diminished in all cases to the lowest values in animals sensitised with IFN-γ after being fed with gliadins and/or bifidobacteria. In these animals, plasma Hamp active peptide concentrations significantly increased when compared with the controls. Significant correlations were calculated between Hamp expression and liver Fe contents (liver Fe = 1/0·0032 + 0·032 x Hamp(exp)), and Hb concentrations (Hb = 11·49 + 10·13 x (Hamp(exp))1/2). These data indicate that oral administration of B. longum ameliorates gliadin-mediated perturbations in liver Fe deposition and mobilisation.
authors: Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain.
authors: José Moisés
authors: JM
authors: Laparra
authors: Marta
authors: M
authors: Olivares
authors: Yolanda
authors: Y
authors: Sanz
mesh_terms: D000284:Administration, Oral; D000740:Anemia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D000818:Animals; D001644:Bifidobacterium; D002446:Celiac Disease / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D005260:Female; D005903:Gliadin / Q000009:adverse effects*; D006454:Hemoglobins / Q000378:metabolism; D064451:Hepcidins / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008286:Malabsorption Syndromes / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D019936:Probiotics / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D011990:Receptors, Transferrin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C578703:Hamp protein, rat; D006454:Hemoglobins; D064451:Hepcidins; D015850:Interleukin-6; D011990:Receptors, Transferrin; C548977:Tfr2 protein, rat; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D005903:Gliadin; D007501:Iron