title: Iron Supplementation Attenuates the Inflammatory Status of Anemic Piglets by Regulating Hepcidin.
abstract: Iron deficiency is common throughout the world and has been linked to immunity impairments. Using piglets to model human infants, we assessed the impact of systemic iron homeostasis on proinflammatory status. Artificially reared piglets were parenterally supplied with iron dextran by intramuscular administration at the age of 3 days. Relative to no iron supplementation (control), iron dextran-treated (FeDex) piglets increased hematological parameters as well as iron levels in serum and tissues from days 21 to 49. High expression of hepcidin was observed in FeDex-treated piglets, which correlated with suppressed expression of ferroportin in duodenum. Lower levels of proinflammatory cytokine (IL-6, TNF-α, IFN-γ, and IL-1β) transcripts were detected in ileum of FeDex-treated piglets, which indicated that iron supplementation could attenuate the increase of inflammatory cytokines caused by iron deficiency. Histopathological analysis of liver and duodenum proved the less inflammatory responses after iron supplementation. Hepcidin was highly stimulated by FeDex supplementation and attenuated the inflammation of anemia, which implied that hepcidin might had antiinflammatory function and is a candidate regulator of the cross-talk between iron regulation and inflammation.
authors.affiliation: Feed Science Institute, College of Animal Science, Zhejiang University, Hangzhou, 310058, People's Republic of China.
authors.forename: Yutian
authors.initials: Y
authors.lastname: Pu
authors.forename: Bingxiu
authors.initials: B
authors.lastname: Guo
authors.forename: Dan
authors.initials: D
authors.lastname: Liu
authors.forename: Haitao
authors.initials: H
authors.lastname: Xiong
authors.forename: Yizhen
authors.initials: Y
authors.lastname: Wang
authors.forename: Huahua
authors.initials: H
authors.lastname: Du
mesh_terms: D000281:Administration, Intranasal; D018798:Anemia, Iron-Deficiency / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D000831:Animals, Newborn; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006397:Hematinics / Q000008:administration & dosage / Q000494:pharmacology; D064451:Hepcidins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007082:Ileum / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D007223:Infant; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D007505:Iron-Dextran Complex / Q000008:administration & dosage / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013552:Swine; D013997:Time Factors; D000098742:Ferroportin
chemical_list: D027682:Cation Transport Proteins; D016207:Cytokines; D006397:Hematinics; D064451:Hepcidins; D018836:Inflammation Mediators; D000098742:Ferroportin; D007505:Iron-Dextran Complex