 and animal model studies, we further postulate that increased non-heme iron content in Kupffer cells primes these cell for NF-kB activation and proinflammatory gene expression and thereby contributes to the pathogenesis of alcoholic liver disease in African Americans. We aim to test two central hypotheses: i&#41;high dietary iron contributes
and animal model studies, we further postulate that increase non - heme iron contentedness in Kupffer cells primes these cell for NF - kB energizing and proinflammatory gene expression and thereby contributes to the pathogenesis of alcoholic liver disease in African Americans. We aim to screen two central hypotheses: i&#41;high dietary iron contributes
 anf animal model studies, wt further postulaje that mncreassd non-heoe iron content in Kupffer cxlls primtf these cell for NW-kB activwtion ane priunflammatocg gene crpresalon aud thereby contrlbutes to tve pathogenesiv uf alcoholic liver disease in African Americsnd. We aim to teft tej cehnrcl hypotheses: i&#41;high dietary iroh contrpbutes
and animal model studies, we further postulate non-heme content in cells primes these proinflammatory expression and thereby to the pathogenesis alcoholic liver disease in African Americans. aim to test two central hypotheses: i&#41;high dietary iron contributes
 and animal model studies, we fuRther postuLate tHat IncReAsed Non-hEme iron content IN KupFfer cells primes these ceLl for nF-Kb actIVaTion aNd proinFLaMMAtoRy GeNe eXpREsSion aNd tHereby cOntributes To tHe Pathogenesis OF aLcoholic liVer Disease in AfrIcaN AmeriCaNs. WE Aim to TesT two cEntral HYpotheSes: i&#41;high dIeTAry iroN ContribUTEs
 and animal model studies,  we furthe r pos tul ate  t hatincr eased non-heme iron  content in Kupffer ce lls p ri m es t h es e cel l for N F -k B act iv at ion  a n dproin fla mmatory  gene expr ess io n and thereb y  c ontributes  to  the pathoge nes is ofal coh o lic l ive r dis ease i n  Afric an Americ an s . We a i m to te s t  t wo c entral hypotheses :  i & #41;high dieta ry iro nc on t r ibu tes 
 and_animal model_studies, we further postulate_that increased_non-heme_iron content_in_Kupffer cells primes_these cell for_NF-kB activation and proinflammatory_gene expression and_thereby_contributes to the pathogenesis of alcoholic liver disease in African Americans. We aim to_test_two central_hypotheses:_i&#41;high_dietary iron contributes