Development of a Vitamin A-deficient mouse model susceptible to Shiga toxin-producing Escherichia Coli infection

CABRERA GABRIEL; ROMINA J. FERNANDEZ-BRANDO; BASCHKIER, ARIELA; MILIWEBSKY, ELIZABETH; MARÍA PILAR MEJÍAS; ABREY RECALDE, MARÍA JIMENA; RIVAS, MARTA; MARINA S. PALERMO

Amsterdam

Congreso; 8th International Symposium on Shiga Toxin (Verocytotoxin) Producing Escgerichi coli Infections; 2012

VTEC

Shiga-toxin (Stx)-producing Escherichia coli (STEC) is a food-borne pathogen that can cause diarrhoea, haemorrhagic colitis and the life-threatening haemolytic uremic syndrome (HUS), a systemic complication that affects to 5-10 % of infected children. Despite important knowledge obtained during last years, several components and mechanisms involved in HUS pathogenesis still remain unclear. An increasing number of reports highlight the critical role of vitamin A (VA) in the maintenance of the gut epithelium and in the homeostasis of the gut-associated lymphoid tissue (GALT). Considering this fact, the aim of this work was to develop a mouse model to study the influence of VA during STEC infection. To generate the VA deficiency, pregnant females were fed a VA-deficient diet since the second week of gestation and the litters received the same diet after weaning. Mice fed a VA-sufficient diet were used as control. Body weights were measured weekly and the level of retinol binding protein 4 (RBP4) in serum was measured monthly by ELISA as a surrogate marker of VA status. We determined that the level of RBP4 decreased progressively from week 8 to 12 in VA-deficient (VA-D) mice: e.g. (mean mg/ml RBP4±SD, n=2) (A) control mice: 32,5±1,9; (B) 12 week-old VA-D mice: 4,75±0,35; p